PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
3140993-14	1988	Our study supports the theory of more than one type of UDP-GT being involved in morphine glucuronidation.	Morphine	80-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
33865918-5	2021	In response to three model pro-genotoxicants: benzo[a]pyrene, Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-aminoanthracene (2-AA),we observed further transcriptional upregulation of xenobiotic metabolising genes (CYP1A1, CYP1A2, NAT1/2, SULT1A2, UGT1A1, UGT1A3) compared to untreated spheroids.	amino-1-methyl-6-phenylimidazo[4,5-b]pyridine	62-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	260-266
807500-1	1975	Reduction in caloric intake was associated with a greater absolute rise in the serum bilirubin concentration in patients with Gilbert"s syndrome and partial hepatic bilirubin uridine diphosphate glucuronyltransferase (UDPG-T) dysfunction compared to patients with hemolytic unconjugated hyperbilirubinemia and normal subjects.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	175-216
33785516-13	2021	Significance Statement The metabolism and excretion of darolutamide in humans revealed that oxidation (CYP3A4) and glucuronidation (UGT1A9, UGT1A1) were the main metabolic routes of elimination.	darolutamide	55-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
34044055-0	2021	In vitro inhibition of human UDP-glucuronosyltransferase (UGT) 1A1 by osimertinib, and prediction of in vivo drug-drug interactions.	osimertinib	70-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-66
34044055-3	2021	High inhibitory effect of osimertinib was shown towards UGT1A1, 1A3, 1A6, 1A7, 1A8, 1A10, 2B7 and 2B15.	osimertinib	26-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
34044055-4	2021	Especially, osimertinib exhibited competitive inhibition against UGT1A1 with a Ki,u of 0.87 +- 0.12 muM.	osimertinib	12-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
34044055-6	2021	Results from quantitative prediction study indicated that osimertinib administered at 80 mg/day may result in a 4.83% increase in the AUC of drugs mainly metabolized by UGT1A1, implying low risk of DDI via liver metabolism.	osimertinib	58-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
34038714-3	2021	Our data indicated that ibrutinib exerted broad inhibition on most of UGTs, including a potent competitive inhibition against UGT1A1 with a Ki value of 0.90 +- 0.03 muM, a noncompetitive inhibition against UGT1A3 and UGT1A7 with Ki values of 0.88 +- 0.03 muM and 2.52 +- 0.23 muM, respectively, while acalabrutinib only exhibited weak UGT inhibition towards all tested UGT isoforms.	ibrutinib	24-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
33877904-0	2021	The Correlation Between UGT1A1 Gene Phenotypes and the Clinical Prognosis of Advanced Colorectal Cancer After FOLFIRI Therapy.	FOLFIRI regimen	110-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
34038714-4	2021	DDI risk prediction suggested that the inhibition against UGT1A1 and UGT1A3 by ibrutinib might bring a potential DDIs risk, while acalabrutinib was unlikely to trigger clinically significant UGT-mediated DDIs due to its weak effects.	ibrutinib	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
33610566-8	2021	Moreover, isobavachalcone demonstrated broad-spectrum inhibitory effects against CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, UGT1A1, UGT1A9, UGT2B7 with IC50 values of 1.08-9.78 muM.	isobavachalcone	10-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
34007799-0	2021	UGT1A1-related Bilirubin Encephalopathy/Kernicterus in Adults.	Bilirubin	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33901188-10	2021	We replicated several proof-of-concept transcriptionally regulated gene-trait associations, including UGT1A1 (encoding bilirubin uridine diphosphate glucuronosyltransferase enzyme) and total bilirubin levels (p = 3.59x10-12), and CETP (cholesteryl ester transfer protein) with high-density lipoprotein cholesterol (p = 4.49x10-12).	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
33901188-10	2021	We replicated several proof-of-concept transcriptionally regulated gene-trait associations, including UGT1A1 (encoding bilirubin uridine diphosphate glucuronosyltransferase enzyme) and total bilirubin levels (p = 3.59x10-12), and CETP (cholesteryl ester transfer protein) with high-density lipoprotein cholesterol (p = 4.49x10-12).	Uridine Diphosphate	129-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
33485974-4	2021	METHODS: RT-qPCR was used to detect the effects of water extract of Polygoni Multiflori Radix (PMR) and its main components on the mRNA expression of CYP3A4 and UGT1A1 in human hepatic parenchyma cell line L02.	Water	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
33485974-18	2021	CONCLUSION: The inhibition of mRNA expression of CYP3A4 or UGT1A1 enhanced hepatotoxicity of PMR.	pmr	93-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
33631237-3	2021	The present study aimed to determine the genotype of the UGT1A1 promoter and exon that are related to the serum total bilirubin (STB) level in the Chinese Han population.	Bilirubin	118-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
33995076-9	2021	Our findings demonstrate that PRH alter expression and function of UGT proteins in an isoform-specific manner and increase UGT1A1-mediated labetalol metabolism in human hepatocytes by inducing UGT1A1 protein concentrations.	Labetalol	139-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
33995076-9	2021	Our findings demonstrate that PRH alter expression and function of UGT proteins in an isoform-specific manner and increase UGT1A1-mediated labetalol metabolism in human hepatocytes by inducing UGT1A1 protein concentrations.	Labetalol	139-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	193-199
33995076-0	2021	Pregnancy-Related Hormones Increase UGT1A1-Mediated Labetalol Metabolism in Human Hepatocytes.	Labetalol	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
33995076-3	2021	Using primary human hepatocytes, we evaluated the effect of PRH exposure on mRNA levels and protein concentrations of UGT1A1, UGT2B7, and other key UGT enzymes, and on the metabolism of labetalol (a UGT1A1 and UGT2B7 substrate commonly prescribed to treat hypertensive disorders of pregnancy).	Labetalol	186-195	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
33830459-6	2021	Cabotegravir is mainly metabolized by UGT1A1, and rilpivirine is mainly metabolized by CYP3A4, therefore these agents are susceptible to DDIs with inhibitors, and particularly inducers of drug-metabolizing enzymes.	cabotegravir	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
33995076-7	2021	PRH exposure also significantly increased labetalol metabolism to its UGT1A1-derived glucuronide metabolite in a concentration-dependent manner, which positively correlated with PRH-induced changes in UGT1A1 protein concentrations.	Labetalol	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
33995076-7	2021	PRH exposure also significantly increased labetalol metabolism to its UGT1A1-derived glucuronide metabolite in a concentration-dependent manner, which positively correlated with PRH-induced changes in UGT1A1 protein concentrations.	Labetalol	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
33995076-7	2021	PRH exposure also significantly increased labetalol metabolism to its UGT1A1-derived glucuronide metabolite in a concentration-dependent manner, which positively correlated with PRH-induced changes in UGT1A1 protein concentrations.	Glucuronides	85-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
33995076-7	2021	PRH exposure also significantly increased labetalol metabolism to its UGT1A1-derived glucuronide metabolite in a concentration-dependent manner, which positively correlated with PRH-induced changes in UGT1A1 protein concentrations.	Glucuronides	85-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
33837924-7	2021	Reports for UGT1A1-metabolized irinotecan and the CYP2C19-metabolized drugs voriconazole, escitalopram and clopidogrel were selected for comparison between the subgroups based upon known genetic polymorphisms with high prevalence in Japan.	Irinotecan	31-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
33733372-3	2021	METHODS: Two pharmacokinetic and one myelosuppression model were assembled to predict concentrations of irinotecan and its metabolite SN-38 given different UGT1A1 genotypes (poor metabolizers: CLSN-38: -36%) and neutropenia following conventional versus PGx-based dosing (350 versus 245 mg/m2 (-30%)).	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
33759451-7	2021	Subsequently, the model was used to explore UGT1A1-related DDI risk with atazanavir and rifampicin along with the effect of enzyme genotype on raltegravir apparent clearance.	Atazanavir Sulfate	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
33759451-7	2021	Subsequently, the model was used to explore UGT1A1-related DDI risk with atazanavir and rifampicin along with the effect of enzyme genotype on raltegravir apparent clearance.	Rifampin	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
33759451-8	2021	Simulations of pregnancy-related induction of UGT1A1 either exacerbated UGT1A1 induction by rifampicin or negated atazanavir UGT1A1 inhibition.	Rifampin	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
33759451-8	2021	Simulations of pregnancy-related induction of UGT1A1 either exacerbated UGT1A1 induction by rifampicin or negated atazanavir UGT1A1 inhibition.	Rifampin	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
33759451-8	2021	Simulations of pregnancy-related induction of UGT1A1 either exacerbated UGT1A1 induction by rifampicin or negated atazanavir UGT1A1 inhibition.	Rifampin	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
33759451-8	2021	Simulations of pregnancy-related induction of UGT1A1 either exacerbated UGT1A1 induction by rifampicin or negated atazanavir UGT1A1 inhibition.	Atazanavir Sulfate	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
33462346-2	2021	DPYD and UGT1A1 variants are relevant predictors of fluoropyrimidine and irinotecan-associated adverse events (AEs).	2-fluoropyrimidine	52-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
33462346-2	2021	DPYD and UGT1A1 variants are relevant predictors of fluoropyrimidine and irinotecan-associated adverse events (AEs).	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
33462346-9	2021	DPYD IVS14+1A allele is confirmed to be associated with fluoropyrimidine life-threatening toxicities, and UGT1A1*28 is related with a higher risk of hematologic AEs following irinotecan treatment.	Irinotecan	175-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
33024987-6	2021	Increases in total bilirubin were more frequently observed in patients treated with enasidenib, consistent with this inhibitor"s known potential to inhibit UGT1A1, but did not appear to have significant clinical consequences.	enasidenib	84-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
33733372-3	2021	METHODS: Two pharmacokinetic and one myelosuppression model were assembled to predict concentrations of irinotecan and its metabolite SN-38 given different UGT1A1 genotypes (poor metabolizers: CLSN-38: -36%) and neutropenia following conventional versus PGx-based dosing (350 versus 245 mg/m2 (-30%)).	Irinotecan	134-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
33290829-3	2021	Belinostat exhibited a wide range of inhibition against UGTs activities, particularly a potent non-competitive inhibition against UGT1A3, and weak inhibition against UGT1A1, 1A7, 1A8, 2B4 and 2B7.	belinostat	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
33790625-0	2021	Influence of UGT1A1 *6/*28 Polymorphisms on Irinotecan-Related Toxicity and Survival in Pediatric Patients with Relapsed/Refractory Solid Tumors Treated with the VIT Regimen.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
33790625-1	2021	Objective: The association between UGT1A1*6/*28 polymorphisms and treatment outcomes of irinotecan in children remains unknown.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
33790625-2	2021	This retrospective study investigated the influence of UGT1A1*6/*28 polymorphisms on irinotecan toxicity and survival of pediatric patients with relapsed/refractory solid tumors.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
33790625-8	2021	Moreover, patients with mutant UGT1A1*6 genotypes were more likely to develop grade I-IV irinotecan-related diarrhea (P = 0.043) and anemia (P = 0.002).	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
33790625-9	2021	Overall, the UGT1A1*28 polymorphism may play a protective role against irinotecan-related diarrhea and abdominal pain.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
33790625-10	2021	Conclusion: In relapsed/refractory pediatric solid tumors, the UGT1A1*6 polymorphism was a risk factor of irinotecan-related diarrhea and anemia.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33790625-11	2021	The UGT1A1*28 polymorphism may serve a protective role in irinotecan-related abdominal pain and diarrhea.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
33386925-0	2021	FOLFIRINOX in advanced pancreatic cancer patients with the double-variant type of UGT1A1 *28 and *6 polymorphism: a multicenter, retrospective study.	folfirinox	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-3	2021	The optimal dose of irinotecan as a component of the FOLFIRINOX has not been established yet for patients with UGT1A1-DV.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
33386925-5	2021	We evaluated the patient characteristics, efficacy and safety of FOLFIRINOX and investigate the optimal initial dose of irinotecan in Japanese advanced PC patients with UGT1A1-DV.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
33619631-0	2021	Effect of UGT1A1, CYP3A and CES Activities on the Pharmacokinetics of Irinotecan and its Metabolites in Patients with UGT1A1 Gene Polymorphisms.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
33619631-0	2021	Effect of UGT1A1, CYP3A and CES Activities on the Pharmacokinetics of Irinotecan and its Metabolites in Patients with UGT1A1 Gene Polymorphisms.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
33619631-2	2021	SN-38 is then converted to the inactive metabolite SN-38 glucuronide (SN-38G) by glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
33619631-2	2021	SN-38 is then converted to the inactive metabolite SN-38 glucuronide (SN-38G) by glucuronosyltransferase 1A1 (UGT1A1).	7-ethyl-10-hydroxycamptothecin glucuronide	51-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
33619631-2	2021	SN-38 is then converted to the inactive metabolite SN-38 glucuronide (SN-38G) by glucuronosyltransferase 1A1 (UGT1A1).	7-ethyl-10-hydroxycamptothecin glucuronide	70-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
33619631-3	2021	Genetic polymorphisms in UGT1A1 have been associated with altered SN-38 pharmacokinetics, which increase the risk of toxicity in patients.	Irinotecan	66-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
33619631-5	2021	We evaluated the activities of UGT1A1, CYP3A, and CES and the factors affecting the pharmacokinetics of plasma SN-38 in patients with UGT1A1 gene polymorphisms.	Irinotecan	111-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
33619631-12	2021	Since UGT1A1 activity was low in patient 1 with a high AUC of SN-38, it can be said that the increase in plasma concentration was due to a decrease in UGT1A1 activity.	Irinotecan	62-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	Irinotecan	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	7-ethyl-10-hydroxycamptothecin glucuronide	86-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	Irinotecan	86-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
33728696-0	2021	UGT1A1 Gene Polymorphisms in Patients with Small Cell Lung Cancer Treated with Irinotecan-Platinum Doublet Chemotherapy and Their Association with Gastrointestinal Toxicity and Overall Survival.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33728696-0	2021	UGT1A1 Gene Polymorphisms in Patients with Small Cell Lung Cancer Treated with Irinotecan-Platinum Doublet Chemotherapy and Their Association with Gastrointestinal Toxicity and Overall Survival.	Platinum	90-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33728696-18	2021	IMPLICATIONS FOR PRACTICE: UGT1A1 gene polymorphisms are known to influence irinotecan-related toxicity.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Platinum	105-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Platinum	105-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Platinum	105-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
33386925-9	2021	CONCLUSION: Based on our findings, we recommend that in Japanese advanced PC patients with UGT1A1- DV treated with FOLFIRINOX, irinotecan be administered at an initial dose of  <= 120 mg/m2.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
33376146-0	2021	Detoxication vs. Bioactivation Pathways of Lapatinib In Vitro: UGT1A1 Catalyzes the Hepatic Glucuronidation of Debenzylated Lapatinib.	Lapatinib	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33376146-0	2021	Detoxication vs. Bioactivation Pathways of Lapatinib In Vitro: UGT1A1 Catalyzes the Hepatic Glucuronidation of Debenzylated Lapatinib.	Lapatinib	124-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33376146-4	2021	In the present study, reaction phenotyping experiments using human recombinant UGT enzymes and enzyme-selective chemical inhibitors demonstrated that UGT1A1 was the major hepatic UGT enzyme involved in lapatinib M1 glucuronidation.	Lapatinib	202-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
33376146-5	2021	Formation of the M1-glucuronide by human liver microsomes from UGT1A1-genotyped donors was significantly correlated with UGT1A1 activity, as measured by 17beta-estradiol 3-glucuronidation (R2 = 0.90).	m1-glucuronide	17-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33376146-5	2021	Formation of the M1-glucuronide by human liver microsomes from UGT1A1-genotyped donors was significantly correlated with UGT1A1 activity, as measured by 17beta-estradiol 3-glucuronidation (R2 = 0.90).	m1-glucuronide	17-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
33376146-5	2021	Formation of the M1-glucuronide by human liver microsomes from UGT1A1-genotyped donors was significantly correlated with UGT1A1 activity, as measured by 17beta-estradiol 3-glucuronidation (R2 = 0.90).	Estradiol	153-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33376146-5	2021	Formation of the M1-glucuronide by human liver microsomes from UGT1A1-genotyped donors was significantly correlated with UGT1A1 activity, as measured by 17beta-estradiol 3-glucuronidation (R2 = 0.90).	Estradiol	153-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
33376146-12	2021	UGT1A1 was identified as the major hepatic enzyme involved in lapatinib M1 glucuronidation, which may limit hepatic exposure to the potentially toxic quinoneimine.	Lapatinib	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33376146-12	2021	UGT1A1 was identified as the major hepatic enzyme involved in lapatinib M1 glucuronidation, which may limit hepatic exposure to the potentially toxic quinoneimine.	quinoneimine	150-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33549631-6	2021	UGT1A1 and -1A10 were inhibited by TPT, whereas UGT 2B4 and -2B7 were inhibited by TBT.	triphenyltin	35-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-16
33549631-10	2021	TPT can additionally inhibit activities of UGT1A1 and -1A10 in estradiol-3-O-glucuronidation, with IC50 values of a few micro-molars.	triphenyltin	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-59
33549631-10	2021	TPT can additionally inhibit activities of UGT1A1 and -1A10 in estradiol-3-O-glucuronidation, with IC50 values of a few micro-molars.	Estradiol	63-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-59
33290829-5	2021	Our data indicate that the intravenous infusion of belinostat at clinical available dose can contribute a significant increase to the AUC of co-administrated drugs primarily cleared by UGT1A3 or UGT1A1, which will result in potential DDIs.	belinostat	51-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	195-201
33263770-3	2021	The effects of a series of di- and trihydroxychalcones as AhR agonists was structure-dependent with maximal induction of CYP1A1, CYP1B1 and UGT1A1 in Caco2 cells observed for compounds containing 2,2"-dihydroxy substituents and this included 2,2"-dihydroxy-, 2,2",4"-trihydroxy- and 2,2",5"-trihydroxychalcones.	di- and trihydroxychalcones	27-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
33263770-3	2021	The effects of a series of di- and trihydroxychalcones as AhR agonists was structure-dependent with maximal induction of CYP1A1, CYP1B1 and UGT1A1 in Caco2 cells observed for compounds containing 2,2"-dihydroxy substituents and this included 2,2"-dihydroxy-, 2,2",4"-trihydroxy- and 2,2",5"-trihydroxychalcones.	2,2"-dihydroxy	196-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
33622223-6	2021	RESULTS: Letermovir was a substrate of CYP3A4/5 and UGT1A1/3 in vitro.	letermovir	9-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-60
33626178-1	2021	Bictegravir is equally metabolized by cytochrome P-450 (CYP)3A and uridine diphosphate-glucuronosyltransferase (UGT)1A1.	bictegravir	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-119
33622223-10	2021	Letermovir inhibited CYP2B6, CYP2C8, CYP3A, and UGT1A1 in vitro, and induced CYP3A4 and CYP2B6 in hepatocytes.	letermovir	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
33685083-1	2021	Objective: To investigate the diagnosis method of Gilbert syndrome (GS) and the relationship between UGT1A1 gene polymorphism distribution with serum bilirubin.	Bilirubin	150-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
33685083-6	2021	Among 110 cases with Gilbert syndrome combined with non-hemolytic diseases, pairwise comparisons showed that the total bilirubin levels of patients with UGT1A1*28/*28 mutations were significantly higher than UGT1A1*6/*6 and UGT1A1*1/*28 + *1/*6 mutation (P < 0.05).	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
33685083-6	2021	Among 110 cases with Gilbert syndrome combined with non-hemolytic diseases, pairwise comparisons showed that the total bilirubin levels of patients with UGT1A1*28/*28 mutations were significantly higher than UGT1A1*6/*6 and UGT1A1*1/*28 + *1/*6 mutation (P < 0.05).	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	208-214
33685083-6	2021	Among 110 cases with Gilbert syndrome combined with non-hemolytic diseases, pairwise comparisons showed that the total bilirubin levels of patients with UGT1A1*28/*28 mutations were significantly higher than UGT1A1*6/*6 and UGT1A1*1/*28 + *1/*6 mutation (P < 0.05).	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	208-214
33685083-7	2021	Additionally, with the increase of UGT1A1*28 distribution, the serum total bilirubin level had gradually increased (P = 0.028), but UGT1A1*6 was opposite (P = 0.021).	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
33628187-3	2020	This study aims to find efficacious UGT1A1 inducer(s) from natural flavonoids, and to reveal the mechanism involved in up-regulating of this key conjugative enzyme by the flavonoid(s) with strong UGT1A1 induction activity.	Flavonoids	67-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
33628187-0	2020	Neobavaisoflavone Induces Bilirubin Metabolizing Enzyme UGT1A1 via PPARalpha and PPARgamma.	neobavaisoflavone	0-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
33551819-7	2020	Conversely, TCDD and OP, the activators of AhR, induced CYP1A1 (38 and 37-fold), and UGT1A1 (4.3 and 5.0-fold), respectively.	Polychlorinated Dibenzodioxins	12-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
33628187-0	2020	Neobavaisoflavone Induces Bilirubin Metabolizing Enzyme UGT1A1 via PPARalpha and PPARgamma.	Bilirubin	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
33628187-1	2020	UDP-glucuronosyltransferase 1A1 (UGT1A1) is an essential enzyme in mammals that is responsible for detoxification and metabolic clearance of the endogenous toxin bilirubin and a variety of xenobiotics, including some crucial therapeutic drugs.	Bilirubin	162-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
33628187-1	2020	UDP-glucuronosyltransferase 1A1 (UGT1A1) is an essential enzyme in mammals that is responsible for detoxification and metabolic clearance of the endogenous toxin bilirubin and a variety of xenobiotics, including some crucial therapeutic drugs.	Bilirubin	162-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
33628187-3	2020	This study aims to find efficacious UGT1A1 inducer(s) from natural flavonoids, and to reveal the mechanism involved in up-regulating of this key conjugative enzyme by the flavonoid(s) with strong UGT1A1 induction activity.	Flavonoids	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
33628187-3	2020	This study aims to find efficacious UGT1A1 inducer(s) from natural flavonoids, and to reveal the mechanism involved in up-regulating of this key conjugative enzyme by the flavonoid(s) with strong UGT1A1 induction activity.	Flavonoids	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
33628187-3	2020	This study aims to find efficacious UGT1A1 inducer(s) from natural flavonoids, and to reveal the mechanism involved in up-regulating of this key conjugative enzyme by the flavonoid(s) with strong UGT1A1 induction activity.	Flavonoids	67-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
33628187-4	2020	Among all the tested flavonoids, neobavaisoflavone (NBIF) displayed the most potent UGT1A1 induction activity, while its inductive effects were confirmed by both western blot and glucuronidation activity assays.	neobavaisoflavone	33-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
33628187-4	2020	Among all the tested flavonoids, neobavaisoflavone (NBIF) displayed the most potent UGT1A1 induction activity, while its inductive effects were confirmed by both western blot and glucuronidation activity assays.	neobavaisoflavone	52-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
33097971-2	2021	Our aim was to assess the efficacy and safety of induction treatment with FOLFOXIRI plus bevacizumab in patients with untreated mCRC harboring UGT1A1 wild (*1/*1), or single-hetero (*1/*6 or *1/*28) genotypes.	folfoxiri	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
33278020-10	2021	Olanzapine and the UDP glucuronosyltransferase family 1 member A1 (UGT1A1) rs887829 polymorphism were associated with elevated glucose levels.	Glucose	127-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-65
33278020-10	2021	Olanzapine and the UDP glucuronosyltransferase family 1 member A1 (UGT1A1) rs887829 polymorphism were associated with elevated glucose levels.	Glucose	127-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
33535454-3	2021	Eudesmin, fargesin, epimagnolin A, magnolin, and yangambin inhibited UGT1A1 and UGT1A3 activities, but showed negligible inhibition of UGT1A4, UGT16, UGT1A9, and UGT2B7 activities at 200 muM in pooled human liver microsomes.	magnolin	20-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
33535454-3	2021	Eudesmin, fargesin, epimagnolin A, magnolin, and yangambin inhibited UGT1A1 and UGT1A3 activities, but showed negligible inhibition of UGT1A4, UGT16, UGT1A9, and UGT2B7 activities at 200 muM in pooled human liver microsomes.	magnolin	23-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
33535454-3	2021	Eudesmin, fargesin, epimagnolin A, magnolin, and yangambin inhibited UGT1A1 and UGT1A3 activities, but showed negligible inhibition of UGT1A4, UGT16, UGT1A9, and UGT2B7 activities at 200 muM in pooled human liver microsomes.	epiyangambin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
33535454-4	2021	Moreover, eudesmin, fargesin, epimagnolin A, magnolin, and yangambin noncompetitively inhibited UGT1A1-catalyzed SN38 glucuronidation with Ki values of 25.7, 25.3, 3.6, 26.0, and 17.1 muM, respectively, based on kinetic analysis of UGT1A1 inhibition in pooled human liver microsomes.	magnolin	30-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
33535454-4	2021	Moreover, eudesmin, fargesin, epimagnolin A, magnolin, and yangambin noncompetitively inhibited UGT1A1-catalyzed SN38 glucuronidation with Ki values of 25.7, 25.3, 3.6, 26.0, and 17.1 muM, respectively, based on kinetic analysis of UGT1A1 inhibition in pooled human liver microsomes.	magnolin	30-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	232-238
33535454-4	2021	Moreover, eudesmin, fargesin, epimagnolin A, magnolin, and yangambin noncompetitively inhibited UGT1A1-catalyzed SN38 glucuronidation with Ki values of 25.7, 25.3, 3.6, 26.0, and 17.1 muM, respectively, based on kinetic analysis of UGT1A1 inhibition in pooled human liver microsomes.	magnolin	33-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
33535454-4	2021	Moreover, eudesmin, fargesin, epimagnolin A, magnolin, and yangambin noncompetitively inhibited UGT1A1-catalyzed SN38 glucuronidation with Ki values of 25.7, 25.3, 3.6, 26.0, and 17.1 muM, respectively, based on kinetic analysis of UGT1A1 inhibition in pooled human liver microsomes.	epiyangambin	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
33535454-4	2021	Moreover, eudesmin, fargesin, epimagnolin A, magnolin, and yangambin noncompetitively inhibited UGT1A1-catalyzed SN38 glucuronidation with Ki values of 25.7, 25.3, 3.6, 26.0, and 17.1 muM, respectively, based on kinetic analysis of UGT1A1 inhibition in pooled human liver microsomes.	epiyangambin	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	232-238
33535454-6	2021	These in vitro results suggest the necessity of evaluating whether the five tetrahydrofurofuranoid lignans can cause drug-drug interactions with UGT1A1 and UGT1A3 substrates in vivo.	tetrahydrofurofuranoid	76-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
33535454-6	2021	These in vitro results suggest the necessity of evaluating whether the five tetrahydrofurofuranoid lignans can cause drug-drug interactions with UGT1A1 and UGT1A3 substrates in vivo.	Lignans	99-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
33615175-9	2021	Further, formation of glucuronides of raloxifene and 7-ethyl-10-hydroxycamptothecin were reduced in the cells expressing the UGT1A1 P152T mutant.	Glucuronides	22-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
33615175-9	2021	Further, formation of glucuronides of raloxifene and 7-ethyl-10-hydroxycamptothecin were reduced in the cells expressing the UGT1A1 P152T mutant.	Raloxifene Hydrochloride	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
33615175-9	2021	Further, formation of glucuronides of raloxifene and 7-ethyl-10-hydroxycamptothecin were reduced in the cells expressing the UGT1A1 P152T mutant.	Irinotecan	53-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
33551819-6	2020	As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively.	6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
33551819-6	2020	As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively.	Phenobarbital	46-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
32648321-12	2020	CONCLUSIONS: CYP1A1 and CYP2C9, UGT1A1, UGT1A7, UGT1A8 and UGT1A9, and MRP4 all played important roles in the metabolism and disposition of bavachin.	bavachin	140-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
33154041-2	2021	However, temporal delay in the development of the UGT1A1 gene leads to an accumulation of serum bilirubin in newborn children.	Bilirubin	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
32813611-0	2021	Main contribution of UGT1A1 and CYP2C9 in the metabolism of UR-1102, a novel agent for the treatment of gout.	UR-1102	60-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
32813611-5	2021	Recombinant UGT1A1 and UGT1A3 showed high glucuronidation of UR-1102.	UR-1102	61-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
33125947-0	2020	Pre-therapeutic UGT1A1 genotyping to reduce the risk of irinotecan-induced severe toxicity: Ready for prime time.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
33125947-1	2020	BACKGROUND: Pre-therapeutic UGT1A1 genotyping is not yet routinely performed in most hospitals in patients starting irinotecan chemotherapy.	Irinotecan	116-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
33125947-5	2020	A high level of evidence (level I) was found for a higher incidence of irinotecan-induced severe toxicity in homozygous carriers of UGT1A1*28 or UGT1A1*6.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
33125947-5	2020	A high level of evidence (level I) was found for a higher incidence of irinotecan-induced severe toxicity in homozygous carriers of UGT1A1*28 or UGT1A1*6.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
33125947-9	2020	CONCLUSION: Pre-therapeutic genotyping of UGT1A1 in patients initiating treatment with irinotecan improves patient safety, is likely to be cost-saving, and should, therefore, become standard of care.	Irinotecan	87-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
33604208-1	2021	Crigler-Najjar syndrome is an inborn error of metabolism caused by a point mutation in one of the five exons of UGT1A1 gene, the product of which is responsible for elimination of bilirubin via bile.	Bilirubin	180-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
33387482-3	2021	Treatment of HepaRG cells with 3-deazaadenosine, an inhibitor of RNA methylation, significantly increased UGT1A1, UGT1A3, UGT1A4, UGT1A9, UGT2B7, UGT2B10, and UGT2B15 mRNA levels (1.3- to 2.6-fold).	3-deazaadenosine	31-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
33119477-1	2020	PURPOSE: Differentiating the irinotecan dose on the basis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) genotype improves the pathologic complete response (pCR) rate.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-112
33119477-1	2020	PURPOSE: Differentiating the irinotecan dose on the basis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) genotype improves the pathologic complete response (pCR) rate.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
33119477-14	2020	CONCLUSION: Adding irinotecan guided by UGT1A1 genotype to capecitabine-based neoadjuvant chemoradiotherapy significantly increased complete tumor response in Chinese patients.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
33201683-5	2020	Coexposure of C3A cells to pentachlorophenol (sulfotransferase 1 inhibitor) or ketoconazole (UDP-glucuronosyltransferase 1A inhibitor) potentiated micronuclei induction by each compound, with thresholds lowered from 2.5-5.0 to 0.6-1.2 muM.	Ketoconazole	79-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-123
32750744-12	2020	CONCLUSIONS: CYP1A2, 2C19 and UGT1As play an important role in isobavachin metabolism.	isobavachin	63-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-34
32750744-8	2020	Additionally, isobavachin underwent efficient oxidation and glucuronidation by human liver microsomes and HIM with CLint values from 5.53 to 148.79 mul/min per mg. CYP1A2, 2C19 contributed 11.3% and 17.1% to hepatic metabolism of isobavachin, respectively, with CLint values from 8.75 to 77.33 mul/min per mg. UGT1As displayed CLint values from 10.73 to 202.62 mul/min per mg for glucuronidation.	isobavachin	14-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	310-314
32750744-9	2020	Besides, significant correlation analysis also proved that CYP1A2, 2C19 and UGT1A1, 1A9 were main contributors for the metabolism of isobavachin.	isobavachin	133-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-87
32750744-11	2020	Moreover, isobavachin exhibited broad inhibition against CYP2B6, 2C9, 2C19, UGT1A1, 1A9, 2B7 with Ki values from 0.05 to 3.05 mum.	isobavachin	10-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
32973940-1	2020	Gilbert syndrome (GS) is a hereditary unconjugated hyperbilirubinemia that results from mutations in the bilirubin uridine diphosphate-glucuronosyltransferase (UGT1A1) gene.	Bilirubin	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
32152464-0	2020	UGT1A1 genotype influences clinical outcome in patients with intermediate-risk acute myeloid leukemia treated with cytarabine-based chemotherapy.	Cytarabine	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
32737884-0	2020	Pharmacogenetic impact of UGT1A1 polymorphisms on pulmonary neuroendocrine tumours treated with metronomic irinotecan-based chemotherapy in Chinese populations.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
32737884-9	2020	Grade 1 total bilirubin elevation was associated with the homozygous UGT1A1*6 mutation (P = 0.027) or any UGT1A1*6 variants (P = 0.047).	Bilirubin	14-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
32737884-9	2020	Grade 1 total bilirubin elevation was associated with the homozygous UGT1A1*6 mutation (P = 0.027) or any UGT1A1*6 variants (P = 0.047).	Bilirubin	14-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
32737884-11	2020	CONCLUSIONS: The impact of UGT1A1 polymorphisms varies in different irinotecan-based chemotherapies.	Irinotecan	68-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
32737884-12	2020	UGT1A1*6 and UGTA1A*28 were useful for the prediction of irinotecan-related severe toxicity in Chinese PNT patients treated with metronomic IBC.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
32152464-4	2020	Here we report the association between the UGT1A1 rs8175347 genotype and the clinical outcome of 455 intermediate-risk cytogenetic AML patients receiving cytarabine-based chemotherapy.	Cytarabine	154-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
32905582-2	2020	In this study, we identified the neuroactive hormone dopamine as an inducer of drug metabolizing enzymes CYP1A1, CYP1B1, and UGT1A1 in colon and glioblastoma cells and similar results were observed for carbidopa.	Dopamine	53-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
32985005-5	2020	In this review, the PGx profiles of drug-gene pairs with potential impact in GI malignancy therapy - DPYD-5-fluorouracil/capecitabine and UGT1A1-irinotecan - and the available clinical evidence of their roles in reducing severe adverse events are discussed.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
32936306-0	2020	Association of UGT1A1*6 polymorphism with irinotecan-based chemotherapy reaction in colorectal cancer patients: a systematic review and a meta-analysis.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
32829105-0	2020	Determination of the UGT1A1 polymorphism as guidance for irinotecan dose escalation in metastatic colorectal cancer treated with first-line bevacizumab and FOLFIRI (PURE FIST).	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
32763815-14	2020	Isozymes of CYP1A2, CYP2C9, UGT1A1, UGT1A6, UGT1A9, UGT2B7 and UGT2B15 were involved in phase I and phase II metabolism of osalmid.	osalmide	123-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
32250470-11	2020	Aripiprazole, dehydro-aripiprazole and olanzapine pharmacokinetics were significantly affected by polymorphisms in CYP2D6, CYP3A, CYP1A2, ABCB1and UGT1A1 genes.	Aripiprazole	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
32250470-11	2020	Aripiprazole, dehydro-aripiprazole and olanzapine pharmacokinetics were significantly affected by polymorphisms in CYP2D6, CYP3A, CYP1A2, ABCB1and UGT1A1 genes.	dehydroaripiprazole	14-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
32250470-11	2020	Aripiprazole, dehydro-aripiprazole and olanzapine pharmacokinetics were significantly affected by polymorphisms in CYP2D6, CYP3A, CYP1A2, ABCB1and UGT1A1 genes.	Olanzapine	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
32829105-0	2020	Determination of the UGT1A1 polymorphism as guidance for irinotecan dose escalation in metastatic colorectal cancer treated with first-line bevacizumab and FOLFIRI (PURE FIST).	FOLFIRI regimen	156-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
32829105-1	2020	AIM: Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility of patients to irinotecan and its toxicity.	Irinotecan	143-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-52
32829105-1	2020	AIM: Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility of patients to irinotecan and its toxicity.	Irinotecan	143-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
32829105-8	2020	CONCLUSION: The current study revealed that mCRC patients, regardless of KRAS gene status, with UGT1A1 genotyping can tolerate escalated doses of irinotecan and potentially achieve a more favourable clinical outcome without significantly increased toxicities.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
33041817-7	2020	In HepG2 cells, hypoxia, KCZ, and RA inhibited CYP450 isoforms and UGT1A1 expression.	Ketoconazole	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
32666389-0	2020	Impact of single-heterozygous UGT1A1 on the clinical outcomes of irinotecan monotherapy after fluoropyrimidine and platinum-based combination therapy for gastric cancer: a multicenter retrospective study.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
32666389-0	2020	Impact of single-heterozygous UGT1A1 on the clinical outcomes of irinotecan monotherapy after fluoropyrimidine and platinum-based combination therapy for gastric cancer: a multicenter retrospective study.	2-fluoropyrimidine	94-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
32666389-0	2020	Impact of single-heterozygous UGT1A1 on the clinical outcomes of irinotecan monotherapy after fluoropyrimidine and platinum-based combination therapy for gastric cancer: a multicenter retrospective study.	Platinum	115-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
32666389-2	2020	We investigated the association between clinical outcomes (efficacy and safety) and UGT1A1 status in patients who received irinotecan monotherapy.	Irinotecan	123-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
33041817-8	2020	Activation of PXR and CAR in cells treated with 6-(4-chlorophenyl)-imidazo (2,1-b) thiazole-5-carbaldehyde (CITCO) and rifampicin (Rif) resulted in the enhancement of CYP450 isoforms, UGT1A1, PXR, and CAR.	6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime	108-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	184-190
33041817-8	2020	Activation of PXR and CAR in cells treated with 6-(4-chlorophenyl)-imidazo (2,1-b) thiazole-5-carbaldehyde (CITCO) and rifampicin (Rif) resulted in the enhancement of CYP450 isoforms, UGT1A1, PXR, and CAR.	6-(4-chlorophenyl)-imidazo (2,1-b) thiazole-5-carbaldehyde	48-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	184-190
32778670-3	2020	Thus, the aim of this study was to assess the allele and genotype frequencies and the relationship between CYP3A4/5, DPYD, UGT1A1, ABCB1, and ABCC2 genetic variations and irinotecan-induced toxicity in Thai colorectal cancer patients.	Irinotecan	171-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
33005200-4	2020	100 muM of kurarinone strongly inhibited more than 90% of UGT1A1, UGT1A6, CYP1A2, and CYP2C9.	kurarinone	11-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
32878631-9	2020	In the MR analysis of the main UGT1A1 SNP (rs6431625), genetically predicted higher levels of total bilirubin were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02-1.12); P = 0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96-1.06); P = 0.73).	Bilirubin	100-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
32829410-5	2021	Associations were characterized with CYP2B6 and UGT1A1 genotypes that affect efavirenz and INSTI metabolism, respectively.	efavirenz	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
32778670-10	2020	This finding suggests that UGT1A1*28, *6, and ABCC2 c.3972C > T might be an important predictor for irinotecan-induced severe neutropenia.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
31495946-5	2020	In patients with complete UGT1A1 deficiency (type 1 CNS [CNS-I]), unconjugated bilirubin levels increase 3-6 mg/dL per day during the newborn period and reach neurologically dangerous levels between 5 and 14 days of age.	Bilirubin	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
32758288-0	2020	UGT1A1 polymorphism has a prognostic effect in patients with stage IB or II uterine cervical cancer and one or no metastatic pelvic nodes receiving irinotecan chemotherapy: a retrospective study.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
32758288-1	2020	BACKGROUND: Uridine diphosphate glucuronosyltransferase 1 family polypeptide A1 (UGT1A1) is a predictive biomarker for the side-effects of irinotecan chemotherapy, which reduces the volume of tumors harboring UGT1A1 polymorphisms.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-79
32758288-1	2020	BACKGROUND: Uridine diphosphate glucuronosyltransferase 1 family polypeptide A1 (UGT1A1) is a predictive biomarker for the side-effects of irinotecan chemotherapy, which reduces the volume of tumors harboring UGT1A1 polymorphisms.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
32361755-0	2020	Evaluation of the effect of UGT1A1 polymorphisms on the pharmacokinetics of oral and long-acting injectable cabotegravir.	cabotegravir	108-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
32361755-2	2020	Cabotegravir is primarily metabolized by uridine 5"-diphospho-glucuronosyltransferase (UGT) 1A1, a known polymorphic enzyme with functional variants that can affect drug metabolism and exposure.	cabotegravir	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-95
32361755-7	2020	A statistically significant (P < 10-5) association between predicted UGT1A1 activity and maximum change in total bilirubin was also observed (2.45-fold asymptomatic increase for low versus normal) without a corresponding change in ALT.	Bilirubin	113-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
32361755-8	2020	CONCLUSIONS: This modest increase in oral and parenteral cabotegravir exposure associated with a reduced function of UGT1A1 is not considered clinically relevant based on accumulated safety data; no dose adjustment is required.	cabotegravir	57-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
32265117-12	2020	CONCLUSION: Our analysis suggested higher completion of concurrent irinotecan was associated with better tumor response for patients with locally advanced rectal cancer with UGT1A1*1*1 or UGT1A1*1*28 phenotypes in the neoadjuvant setting, and at least 4 cycles was recommended.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
32265117-12	2020	CONCLUSION: Our analysis suggested higher completion of concurrent irinotecan was associated with better tumor response for patients with locally advanced rectal cancer with UGT1A1*1*1 or UGT1A1*1*28 phenotypes in the neoadjuvant setting, and at least 4 cycles was recommended.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
32179043-4	2020	Since the knockdown of UDP-glucose 6-dehydrogenase, a synthetase of UDPGA, in HEK293 cells stably expressing UGT1A1 (HEK/UGT1A1 cells) resulted in a significant decrease in 4-methylumbelliferone (4-MU) glucuronosyltransferase activity, supplementation of a sufficient amount of UDPGA is required for UGT activity.	Hymecromone	173-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
32011683-0	2020	Genetic influence of ABCG2, UGT1A1 and NR1I2 on dolutegravir plasma pharmacokinetics.	dolutegravir	48-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
32011683-2	2020	We sought to ascertain the contributory effect of SNPs in four key genes linked to dolutegravir disposition (UGT1A1, ABCG2, CYP3A and NR1I2) on plasma dolutegravir pharmacokinetics.	dolutegravir	83-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
32011683-2	2020	We sought to ascertain the contributory effect of SNPs in four key genes linked to dolutegravir disposition (UGT1A1, ABCG2, CYP3A and NR1I2) on plasma dolutegravir pharmacokinetics.	dolutegravir	151-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
32011683-8	2020	CONCLUSIONS: This study showed a pharmacogenetic association between dolutegravir pharmacokinetics and variants in the ABCG2, UGT1A1 and NR1I2 genes, particularly when combined.	dolutegravir	69-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
32758288-1	2020	BACKGROUND: Uridine diphosphate glucuronosyltransferase 1 family polypeptide A1 (UGT1A1) is a predictive biomarker for the side-effects of irinotecan chemotherapy, which reduces the volume of tumors harboring UGT1A1 polymorphisms.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
32758288-2	2020	We aimed to determine whether UGT1A1 polymorphisms can predict progression-free survival in patients with local cervical cancer treated with irinotecan chemotherapy.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
32758288-10	2020	Among patients with <=1 metastatic lymph node, those with UGT1A1 polymorphisms benefited from irinotecan chemotherapy and demonstrated significantly longer progression-free survival (p = 0.020) than those with wild-type UGT1A1.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
32758288-11	2020	CONCLUSIONS: Irinotecan chemotherapy might be beneficial in patients with cervical cancer, UGT1A1 polymorphisms, and <= 1 metastatic lymph nodes.	Irinotecan	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
32850329-8	2020	Pharmacogenomic analyses revealed multiple alterations of fluoropyrimidine and irinotecan metabolism: severe deficiency of fluorouracil degradation rate (FUDR), single nucleotide polymorphisms of UGT1A1 *28 variable number of tandem repeats (VNTR) 7R/7R homozygote, ABCB1 c.C3435T, c.C1236T, MTHFR c.C667T homozygote, DPYD c.A166G, TSER 28bp VNTR 2R/3R heterozygote.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
34007623-0	2020	Dosage Adjustment of Irinotecan in Patients with UGT1A1 Polymorphisms: A Review of Current Literature.	Irinotecan	21-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
34007623-1	2020	Objective: To review available literature regarding pharmacogenomics (PGx) effects on the metabolism of irinotecan by the UGT1A1 gene and the resulting dose adjustments based on PGx genetic variant.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
34007623-3	2020	The extent of decreased function of UGT1A1 varies based on genotype so irinotecan dose adjustments may be needed.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
34007623-7	2020	Conclusion: These findings add to a growing body of literature that suggest patients with UGT1A1 *28 or *6 variant alleles benefit from lower doses of irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
32612873-1	2020	The human UDP-glucuronosyltransferase 1A1 (UGT1A1), one of the most essential conjugative enzymes, is responsible for the metabolism and detoxification of bilirubin and other endogenous substances, as well as many different xenobiotic compounds.	Bilirubin	155-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-41
32612873-1	2020	The human UDP-glucuronosyltransferase 1A1 (UGT1A1), one of the most essential conjugative enzymes, is responsible for the metabolism and detoxification of bilirubin and other endogenous substances, as well as many different xenobiotic compounds.	Bilirubin	155-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
32264830-0	2020	Correlation between UGT1A1 gene polymorphism and irinotecan chemotherapy in metastatic colorectal cancer: a study from Guangxi Zhuang.	Irinotecan	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
32264830-14	2020	The UGT1A1 gene polymorphism with irinotecan chemotherapy-associated diarrhea and neutropenia were closely related.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
31980500-3	2020	The expression of UGT1A1 is developmentally delayed in liver and intestines resulting in the accumulation of serum bilirubin during the neonatal period.	Bilirubin	115-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
31233374-10	2020	Glucuronidation of glycyrol was primarily mediated by UGT1A1, UGT1A3, UGT1A9, and UGT2B7.	glycyrol	19-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
32323779-0	2020	Sulforaphane suppresses carcinogenesis of colorectal cancer through the ERK/Nrf2-UDP glucuronosyltransferase 1A metabolic axis activation.	sulforaphane	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-111
32323779-2	2020	The detoxification of CRC food-borne carcinogenic heterocyclic amines is highly dependent on UDP glucuronosyltransferase 1A (UGT1A)-mediated glucuronidation.	Amines	63-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-123
32323779-2	2020	The detoxification of CRC food-borne carcinogenic heterocyclic amines is highly dependent on UDP glucuronosyltransferase 1A (UGT1A)-mediated glucuronidation.	Amines	63-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-130
32323779-10	2020	Reverse transcription-quantitative polymerase chain reaction and western blotting were employed to verify the role of Nrf2 in SFN-induced UGT1A.	sulforaphane	126-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-143
32323779-17	2020	Pretreatment with PD58059 reversed the SFN-induced subcellular translocation of Nrf2 and the expression of UGT1A.	pd58059	18-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-112
30514181-4	2020	Irinotecan is bioactivated into its metabolite SN-38, which is subsequently detoxified by uridine diphosphate-glucuronosyl transferases (mainly UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
30514181-4	2020	Irinotecan is bioactivated into its metabolite SN-38, which is subsequently detoxified by uridine diphosphate-glucuronosyl transferases (mainly UGT1A1).	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
31233374-12	2020	In conclusion, glycyrol undergoes the efficient metabolic hydroxylation and glucuronidation reactions in human liver microsomes, which are predominantly catalyzed by CYP1A2, UGT1A1/3/9, and UGT2B7.	glycyrol	15-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
31888882-8	2020	After stratification by UGT1A1 phenotypes, there was a significant decrease in total bilirubin among all phenotypes, conjugated bilirubin among intermediate metabolizers, and unconjugated bilirubin among normal and intermediate metabolizers.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
31602632-10	2020	Homozygosity (41%) for the promoter variant of UGT1A1 (Gilbert syndrome) led to a significantly higher mean bilirubin level (126 54 micromol/l) with a higher frequency of cholelithiasis (30%) (P &lt; 0 001).	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
32131538-5	2020	These in vitro DDI potentials of mertansine with CYP1A2, CYP2B6, CYP2C8/9/19, CYP3A4, UGT1A1, and UGT1A9 substrates suggest that it is necessary to carefully characterize the DDI potentials of ADC candidates with mertansine as a payload in the clinic.	Maytansine	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
31888882-8	2020	After stratification by UGT1A1 phenotypes, there was a significant decrease in total bilirubin among all phenotypes, conjugated bilirubin among intermediate metabolizers, and unconjugated bilirubin among normal and intermediate metabolizers.	Bilirubin	128-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
31888882-8	2020	After stratification by UGT1A1 phenotypes, there was a significant decrease in total bilirubin among all phenotypes, conjugated bilirubin among intermediate metabolizers, and unconjugated bilirubin among normal and intermediate metabolizers.	Bilirubin	128-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
31888882-9	2020	The data also show that UGT1A1 genotype predicts serum bilirubin levels at baseline, but this relationship is lost after efavirenz treatment.	Bilirubin	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
31888882-11	2020	Our data suggest that efavirenz may alter bilirubin disposition mainly through induction of UGT1A1 metabolism and efflux through multidrug resistance-associated protein 2.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
31812603-4	2020	Our data indicated that PT exhibited potent inhibition against HLM, UGT1A6, UGT1A9, UGT2B7, and UGT2B15, moderate inhibition against UGT1A1, UGT1A3, UGT1A8, and UGT2B4, negligible inhibition against UGT1A4, UGT1A7, UGT1A10, and UGT2B17.	pterostilbene	24-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
32058557-2	2020	Evaluation of pharmacogenomically dosed perioperative gFOLFIRINOX (fluorouracil, leucovorin, oxaliplatin, and UGT1A1 genotype-directed irinotecan) to optimize efficacy while limiting toxic effects may have value.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
32204767-2	2020	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1), organic anion transporter polypeptide 2 (OATP2), heme oxygenase 1 (HO-1), and biliverdin reductase A (BLVRA) play crucial roles in the metabolism of bilirubin.	Bilirubin	207-216	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-47
31691077-4	2020	Our data indicated that sunitinib exhibited competitive inhibition against SN-38 glucuronidation by UGT1A1, but inhibitory effects of sunitinib were weak in pooled human liver microsomes (HLMs) (Ki = 119.00 muM) and recombinant UGT1A1 (Ki = 42.71 muM).	sunitinib	24-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
31691077-4	2020	Our data indicated that sunitinib exhibited competitive inhibition against SN-38 glucuronidation by UGT1A1, but inhibitory effects of sunitinib were weak in pooled human liver microsomes (HLMs) (Ki = 119.00 muM) and recombinant UGT1A1 (Ki = 42.71 muM).	sunitinib	24-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	228-234
31640912-0	2020	Pazopanib-Induced Liver Toxicity in Patients With Metastatic Renal Cell Carcinoma: Effect of UGT1A1 Polymorphism on Pazopanib Dose Reduction, Safety, and Patient Outcomes.	pazopanib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
31640912-11	2020	Patients with UGT1A1 polymorphism safely resumed pazopanib at ultra-low doses determined by the degree of liver toxicity and UGT1A1 polymorphism.	pazopanib	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
31640912-11	2020	Patients with UGT1A1 polymorphism safely resumed pazopanib at ultra-low doses determined by the degree of liver toxicity and UGT1A1 polymorphism.	pazopanib	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
31640912-13	2020	UGT1A1 assessment could improve the management of pazopanib-induced liver toxicity in patients with mRCC.	pazopanib	50-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
31525573-2	2020	The elimination of RAL to RAL glucuronide (RAL GLU) is mediated primarily by UDP glucuronosyltransferase 1A1 (UGT1A1).	Glucuronides	30-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-108
32049823-9	2020	Serum TB correlated positively with UGT1A1 mutation load (gamma = 0.281, P = .048), hemoglobin (gamma = .359, P = .010) and hematocrit (gamma = 0.365, P = .010), but negatively with RBC lifespan (gamma = -0.336, P = .017).	Bilirubin	6-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
32433020-11	2020	Distinct expression of UGT1A1, CYP2B6, CYP2C9, CYP3A4, and CYP7A1 genes explains the ability to clear toxins and bilirubin as observed in normal hepatocytes.	Bilirubin	113-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
31727359-8	2020	With silymarin, we found that UGT1A1 and, to a lesser extent UGT1A9, were primarily responsible for the glucuronidation of the flavonolignan constituents.	Flavonolignans	127-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
31727359-9	2020	It is concluded that the metabolism of silymarin flavonolignans may involve multiple UGT enzymes, of which UGT1A1 appears to play the major role in the glucuronidation.	Flavonolignans	39-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
31965023-7	2020	HLSC expressed UGT1A1 in vivo, induced a strong decrease in serum unconjugated bilirubin, thus significantly improving phenotype and survival compared to untreated controls.	Bilirubin	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
31525573-2	2020	The elimination of RAL to RAL glucuronide (RAL GLU) is mediated primarily by UDP glucuronosyltransferase 1A1 (UGT1A1).	Glucuronides	30-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
31525573-2	2020	The elimination of RAL to RAL glucuronide (RAL GLU) is mediated primarily by UDP glucuronosyltransferase 1A1 (UGT1A1).	Glutamic Acid	47-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-108
31525573-2	2020	The elimination of RAL to RAL glucuronide (RAL GLU) is mediated primarily by UDP glucuronosyltransferase 1A1 (UGT1A1).	Glutamic Acid	47-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
31740989-5	2020	In agreement with our previous genotyping data, the genetic polymorphism of uridine 5"-diphospho-glucuronosyltransferase (UGT)1A1*6, which affects the glucuronidation activity and circulating glucuronic acid level was identified as one of the determinants of MMI-induced hepatotoxicity.	Uridine	76-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
31740989-5	2020	In agreement with our previous genotyping data, the genetic polymorphism of uridine 5"-diphospho-glucuronosyltransferase (UGT)1A1*6, which affects the glucuronidation activity and circulating glucuronic acid level was identified as one of the determinants of MMI-induced hepatotoxicity.	Glucuronic Acid	192-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
32237326-1	2020	The bilirubin metabolism mediated by the phase II metabolizing enzyme UGT1A1 in the liver was evaluated to study the potential hepatotoxicity risk based on investigation on the inhibitory effect of rhein and its metabolites on the UGT1A1 enzyme in Rhei Radix et Rhizoma.	Bilirubin	4-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
31707444-8	2020	CONCLUSIONS: The disposition of PEGylated SN-38 is independent of UGT1A activity in rats, and PLX038 may find utility in full-dose treatment of patients who are UGT1A1*28 homozygotes or have metastatic disease with coincidental or incidental liver dysfunction.	5-(1H-pyrrolo(2,3-b)pyridin-3-ylmethyl)-N-((4-(trifluoromethyl)phenyl)methyl)pyridin-2-amine	94-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
33622990-2	2020	This polymorphism leads to 30% of normal rate transcription initiation of UGT1A1 gene, thus decreasing the bilirubin glucuronidation.	Bilirubin	107-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
31342573-6	2020	The transplanted pHSCs underwent maturation in vivo to restore the deficient metabolic hepatic function (bilirubin glucuronidation by UGT1A1).	Bilirubin	105-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
31558477-0	2020	Clinical Assessment of 5-Fluorouracil/Leucovorin, Nab-Paclitaxel, and Irinotecan (FOLFIRABRAX) in Untreated Patients with Gastrointestinal Cancer Using UGT1A1 Genotype-Guided Dosing.	Fluorouracil	23-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
31558477-0	2020	Clinical Assessment of 5-Fluorouracil/Leucovorin, Nab-Paclitaxel, and Irinotecan (FOLFIRABRAX) in Untreated Patients with Gastrointestinal Cancer Using UGT1A1 Genotype-Guided Dosing.	folfirabrax	82-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	48-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	48-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
31558477-4	2020	We performed a trial to assess the safety and tolerability of FOLFIRABRAX with UGT1A1 genotype-guided dosing of irinotecan.	folfirabrax	62-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
31558477-4	2020	We performed a trial to assess the safety and tolerability of FOLFIRABRAX with UGT1A1 genotype-guided dosing of irinotecan.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
31558477-16	2020	CONCLUSIONS: FOLFIRABRAX with genotype-guided dosing of irinotecan is tolerable in patients with advanced gastrointestinal cancer and UGT1A1*1*1 or UGT1A1*1*28 genotypes.	folfirabrax	13-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
31558477-16	2020	CONCLUSIONS: FOLFIRABRAX with genotype-guided dosing of irinotecan is tolerable in patients with advanced gastrointestinal cancer and UGT1A1*1*1 or UGT1A1*1*28 genotypes.	folfirabrax	13-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
31558477-16	2020	CONCLUSIONS: FOLFIRABRAX with genotype-guided dosing of irinotecan is tolerable in patients with advanced gastrointestinal cancer and UGT1A1*1*1 or UGT1A1*1*28 genotypes.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
31558477-16	2020	CONCLUSIONS: FOLFIRABRAX with genotype-guided dosing of irinotecan is tolerable in patients with advanced gastrointestinal cancer and UGT1A1*1*1 or UGT1A1*1*28 genotypes.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
31254178-0	2019	Effects of UGT1A1 Polymorphism, Gender and Triglyceride on the Pharmacokinetics of Telmisartan in Chinese Patients with Hypertension: A Population Pharmacokinetic Analysis.	Telmisartan	83-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
31254178-3	2019	In this study, we aimed to develop a population pharmacokinetic (PopPK) model to quantify the effects of gender and UGT1A1 polymorphisms on the pharmacokinetics of telmisartan.	Telmisartan	164-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
31254178-9	2019	UGT1A1 (rs4124874) affected the bioavailability (F1) of telmisartan.	Telmisartan	56-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
31254178-11	2019	CONCLUSION: A PopPK model of telmisartan was established to confirm that UGT1A1 genotype, gender and triglyceride can affect the pharmacokinetics of telmisartan in Chinese patients with hypertension.	Telmisartan	29-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
31254178-11	2019	CONCLUSION: A PopPK model of telmisartan was established to confirm that UGT1A1 genotype, gender and triglyceride can affect the pharmacokinetics of telmisartan in Chinese patients with hypertension.	Telmisartan	149-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
31586129-1	2019	It has been reported that there are differences in effects on irinotecan-induced adverse reactions between UGT1A1*6 and UGT1A1*28.	irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
31586129-1	2019	It has been reported that there are differences in effects on irinotecan-induced adverse reactions between UGT1A1*6 and UGT1A1*28.	irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
31586129-2	2019	In order to compare those differences in the Japanese population, we examined the associations between UGT1A1 and irinotecan-induced adverse reactions using the BioBank Japan Project database.	irinotecan	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
31730632-2	2019	For example, adverse drug reactions when patients receive CPT-11 (irinotecan) such as in cancer chemotherapy are caused by amino acid substitutions in UGT1A1.	irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
31621310-2	2019	Therefore, we examined the structure-activity relationships of isoflavones and isomeric flavone and flavanones as AhR ligands on the basis of their induction of CYP1A1, CYP1B1, and UGT1A1 gene expression in colon cancer Caco2 cells and young adult mouse colonocyte (YAMC) cells.	Isoflavones	63-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-187
31621310-2	2019	Therefore, we examined the structure-activity relationships of isoflavones and isomeric flavone and flavanones as AhR ligands on the basis of their induction of CYP1A1, CYP1B1, and UGT1A1 gene expression in colon cancer Caco2 cells and young adult mouse colonocyte (YAMC) cells.	Flavanones	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-187
31621310-5	2019	For example, 4",5,7-trihydroxyisoflavone (genistein) was AhR-inactive whereas 4",5,7-trihydroxyflavone (apigenin) induced CYP1A1, CYP1B1, and UGT1A1 in Caco2 cells.	5,7,4'-trihydroxyflavone	78-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
31621310-5	2019	For example, 4",5,7-trihydroxyisoflavone (genistein) was AhR-inactive whereas 4",5,7-trihydroxyflavone (apigenin) induced CYP1A1, CYP1B1, and UGT1A1 in Caco2 cells.	Apigenin	104-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
31730632-5	2019	We then derived a mathematical model that can predict the conjugation capacities of mutant UGT1A1s by using results of substrate docking in silico and results of in vitro analysis of glucuronidation of acetaminophen and 17beta-estradiol by UGT1A1s.	Acetaminophen	202-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
31730632-5	2019	We then derived a mathematical model that can predict the conjugation capacities of mutant UGT1A1s by using results of substrate docking in silico and results of in vitro analysis of glucuronidation of acetaminophen and 17beta-estradiol by UGT1A1s.	Acetaminophen	202-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	240-246
31730632-5	2019	We then derived a mathematical model that can predict the conjugation capacities of mutant UGT1A1s by using results of substrate docking in silico and results of in vitro analysis of glucuronidation of acetaminophen and 17beta-estradiol by UGT1A1s.	Estradiol	220-236	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
31730632-6	2019	This experimental procedure showed that the in silico conjugation capacities of other mutant UGT1A1s with bilirubin or SN-38 were similar to reported in vitro conjugation capacities.	Bilirubin	106-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
31715674-8	2019	Conclusions: The related gene UGT1A1 is related to the metabolism of thyroxine in the liver.	Thyroxine	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
31715674-11	2019	Abnormal serum thyroxine levels during pregnancy may be associated with abnormal metabolism of thyroxine caused by UGT1A1 mutation.	Thyroxine	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
31715674-11	2019	Abnormal serum thyroxine levels during pregnancy may be associated with abnormal metabolism of thyroxine caused by UGT1A1 mutation.	Thyroxine	95-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
31445021-6	2019	The structures of dabrafenib, ibrutinib, lapatinib, nintedanib, pazopanib, regorafenib, trametinib and 22 other KIs overlaid well on that of sorafenib, a potent inhibitor of UGT1A1 and UGTs 1A7-1A10.	Sorafenib	141-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
31840682-6	2019	Thus, potent inducers of UGT1A1 and CYP3A4 (e.g., rifamycins/anticonvulsants) should be avoided due to significantly decreased BIC serum exposure.	rifamycin S	50-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
31445021-1	2019	We have demonstrated previously that the kinase inhibitors (KIs) lapatinib, pazopanib, regorafenib and sorafenib are potent inhibitors of UGT1A1 and UGTs 1A7-1A10.	Lapatinib	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
31445021-1	2019	We have demonstrated previously that the kinase inhibitors (KIs) lapatinib, pazopanib, regorafenib and sorafenib are potent inhibitors of UGT1A1 and UGTs 1A7-1A10.	pazopanib	76-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
31445021-1	2019	We have demonstrated previously that the kinase inhibitors (KIs) lapatinib, pazopanib, regorafenib and sorafenib are potent inhibitors of UGT1A1 and UGTs 1A7-1A10.	regorafenib	87-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
31445021-1	2019	We have demonstrated previously that the kinase inhibitors (KIs) lapatinib, pazopanib, regorafenib and sorafenib are potent inhibitors of UGT1A1 and UGTs 1A7-1A10.	Sorafenib	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
31445021-3	2019	Dabrafenib, ibrutinib, nintedanib and trametinib were potent inhibitors of human liver microsomal UGT1A1; Ki,u values ranged from 1.1 to 7.5 microM.	dabrafenib	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
31445021-3	2019	Dabrafenib, ibrutinib, nintedanib and trametinib were potent inhibitors of human liver microsomal UGT1A1; Ki,u values ranged from 1.1 to 7.5 microM.	ibrutinib	12-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
31445021-3	2019	Dabrafenib, ibrutinib, nintedanib and trametinib were potent inhibitors of human liver microsomal UGT1A1; Ki,u values ranged from 1.1 to 7.5 microM.	nintedanib	23-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
31445021-3	2019	Dabrafenib, ibrutinib, nintedanib and trametinib were potent inhibitors of human liver microsomal UGT1A1; Ki,u values ranged from 1.1 to 7.5 microM.	trametinib	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
31840682-6	2019	Thus, potent inducers of UGT1A1 and CYP3A4 (e.g., rifamycins/anticonvulsants) should be avoided due to significantly decreased BIC serum exposure.	bictegravir	127-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
31207516-8	2019	At concentrations relevant for human exposure (ng/mL range) BPA and its analogues as individual compounds and in mixtures did not exert genotoxic activity, whereas BPA and BPAF as well as the mixtures up-regulated the expressions of CYP1A1 and UGT1A1.	bisphenol A	164-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	244-250
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorooctanoic acid	213-235	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorooctanoic acid	237-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorododecanoic acid	247-271	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorododecanoic acid	273-278	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-11	2019	PFDA and PFOS exhibited competitive inhibition towards UGT1A1, and PFDA and PFTA showed competitive inhibition towards UGT1A8.	perfluorodecanoic acid	0-4	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
31472452-11	2019	PFDA and PFOS exhibited competitive inhibition towards UGT1A1, and PFDA and PFTA showed competitive inhibition towards UGT1A8.	perfluorooctane sulfonic acid	9-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
31472452-13	2019	The values were calculated to be 0.3 mumoL/L and 1.3 mumoL/L for the in vivo inhibition of PFDA towards UGT1A1-and UGT1A8-catalyzed metabolism of substances, and 0.2 mumoL/L and 2.0 mumoL/L for the inhibition of PFOS towards UGT1A1 and the inhibition of PFTA towards UGT1A8, respectively.	perfluorodecanoic acid	91-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
31472452-13	2019	The values were calculated to be 0.3 mumoL/L and 1.3 mumoL/L for the in vivo inhibition of PFDA towards UGT1A1-and UGT1A8-catalyzed metabolism of substances, and 0.2 mumoL/L and 2.0 mumoL/L for the inhibition of PFOS towards UGT1A1 and the inhibition of PFTA towards UGT1A8, respectively.	perfluorodecanoic acid	91-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	225-231
31554401-5	2019	(2R)-8-PN was a better substrate for all 11 UGTs except for UGT1A1, which formed more of both (2S)-8-PN glucuronides than (2R)-8-PN glucuronides.	8-prenylnaringenin	94-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
31554401-5	2019	(2R)-8-PN was a better substrate for all 11 UGTs except for UGT1A1, which formed more of both (2S)-8-PN glucuronides than (2R)-8-PN glucuronides.	8-prenylnaringenin	122-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorodecanoic acid	94-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorodecanoic acid	118-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	Potassium perfluorooctanesulfonate	125-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	perfluorooctane sulfonic acid	170-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	Perfluorotetradecanoic acid	177-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31472452-7	2019	The activity of UGT1A1 was inhibited by 98.8%, 98%, 79.9%, 77.1%, and 76.9% at 100 mumoL/L of perfluorodecanoic acid (PFDA), perfluorooctanesulfonic acid potassium salt (PFOS), perfluorotetradecanoic acid (PFTA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), respectively.	pifithrin	206-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
31619193-0	2019	Uridine diphosphate glucuronosyl transferase 1A (UGT1A1) promoter polymorphism in young patients with sickle cell anaemia: report of the first cohort study from Nigeria.	Uridine Diphosphate	0-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
31619193-1	2019	BACKGROUND: (TA) n repeat sequence (rs8175347) of UGT1A1 gene promoter polymorphism is associated with serum bilirubin levels and gallstones among different sickle cell anaemia (SCA) populations.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
31619193-13	2019	Although, bilirubin and fetal hemoglobin (HbF) of patients with gallstones were significantly different from those without gallstone, only the serum bilirubin was associated with UGT1A1 (TA) n genotypes on multivariate analysis (p &lt; 0.0001).	Bilirubin	149-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
31207516-8	2019	At concentrations relevant for human exposure (ng/mL range) BPA and its analogues as individual compounds and in mixtures did not exert genotoxic activity, whereas BPA and BPAF as well as the mixtures up-regulated the expressions of CYP1A1 and UGT1A1.	4,4'-hexafluorisopropylidene diphenol	172-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	244-250
30484368-6	2019	The half-maximal inhibitory concentration (IC50) of PTL on the activity of UGT1A1 was determined to be 64.4 muM.	parthenolide	52-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
31649539-11	2019	Similarities in allele frequency, comparing major continental groups for VIP pharmacogenes, hint towards a comparable PGx for drugs metabolized by UGT1A1, DPYD, ABCB1, CBR3, COMT, and TPMT; in contrast to variants on CYP3A5 and CYP2B6 for which significant MAF differences were identified.	Epoprostenol	118-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
30484368-7	2019	Inhibition kinetics determination showed that PTL exerted noncompetitive inhibition toward UGT1A1, and the inhibition kinetic constant (Ki) was determined to be 12.1 muM.	parthenolide	46-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
30484368-8	2019	In silico docking method has been employed to show that hydrogen bonds between PTL and the activity cavity of UGT1A1 contributed to the stronger inhibition of PTL on the activity of UGT1A1 than MCL.	Hydrogen	56-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
30484368-8	2019	In silico docking method has been employed to show that hydrogen bonds between PTL and the activity cavity of UGT1A1 contributed to the stronger inhibition of PTL on the activity of UGT1A1 than MCL.	Hydrogen	56-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
30484368-8	2019	In silico docking method has been employed to show that hydrogen bonds between PTL and the activity cavity of UGT1A1 contributed to the stronger inhibition of PTL on the activity of UGT1A1 than MCL.	parthenolide	79-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
30484368-8	2019	In silico docking method has been employed to show that hydrogen bonds between PTL and the activity cavity of UGT1A1 contributed to the stronger inhibition of PTL on the activity of UGT1A1 than MCL.	parthenolide	79-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
30484368-9	2019	In conclusion, PTL can more easily induce drug-drug interaction (DDI) with clinical drugs mainly undergoing UGT1A1-catalyzed glucuronidation.	parthenolide	15-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
31128210-6	2019	The further enzyme kinetic studies demonstrated that shikonin was not only a competitive inhibitor of human UGT1A1, UGT1A9, and UGT2B7, but also presented competitive inhibition on rat UGT1A1 and AZTG reactions.	shikonin	53-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
31611795-0	2019	Oleanolic Acid and Ursolic Acid Induce UGT1A1 Expression in HepG2 Cells by Activating PXR Rather Than CAR.	Oleanolic Acid	0-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
31611795-0	2019	Oleanolic Acid and Ursolic Acid Induce UGT1A1 Expression in HepG2 Cells by Activating PXR Rather Than CAR.	ursolic acid	19-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
31611795-6	2019	Results: In HepG2 cells, OA and UA both significantly induced the expression of UGT1A1, UGT1A3, UGT1A4, and UGT1A9 and upregulated the expression of PXR.	Oleanolic Acid	25-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
31611795-6	2019	Results: In HepG2 cells, OA and UA both significantly induced the expression of UGT1A1, UGT1A3, UGT1A4, and UGT1A9 and upregulated the expression of PXR.	ursolic acid	32-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
31611795-8	2019	A dual-luciferase reporter assay showed that OA and UA could markedly promote PXR-mediated UGT1A1 luciferase activity, whereas OA and UA did not affect CAR-mediated UGT1A1 luciferase activity.	Oleanolic Acid	45-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
31611795-8	2019	A dual-luciferase reporter assay showed that OA and UA could markedly promote PXR-mediated UGT1A1 luciferase activity, whereas OA and UA did not affect CAR-mediated UGT1A1 luciferase activity.	ursolic acid	52-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
31611795-10	2019	However, the expression of UGT1A1 in hCAR-silenced HepG2 cells was markedly elevated compared to the control group or with non-silenced HepG2 cells treated with OA (10, 20, and 40 muM) or UA (10, 20, and 40 muM).	Oleanolic Acid	161-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
31611795-10	2019	However, the expression of UGT1A1 in hCAR-silenced HepG2 cells was markedly elevated compared to the control group or with non-silenced HepG2 cells treated with OA (10, 20, and 40 muM) or UA (10, 20, and 40 muM).	ursolic acid	188-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
31611795-11	2019	Conclusions: OA and UA significantly induce the expression of UGT1A1, UGT1A3, UGT1A4, and UGT1A9 in HepG2 cells, and their induction on UGT1A1 is mediated by PXR activation, not CAR.	Oleanolic Acid	13-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
31611795-11	2019	Conclusions: OA and UA significantly induce the expression of UGT1A1, UGT1A3, UGT1A4, and UGT1A9 in HepG2 cells, and their induction on UGT1A1 is mediated by PXR activation, not CAR.	ursolic acid	20-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
31022310-0	2019	Pharmacogenetic Analysis of OATP1B1, UGT1A1, and BCRP Variants in Relation to the Pharmacokinetics of Letermovir in Previously Conducted Clinical Studies.	letermovir	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
30588615-3	2019	Uridine 5"-diphospho-glucuronosyl transferase (UGT)1A1 variants coding for bilirubin UDP-glucuronosyl transferase resulting in mild hyperbilirubinemia (as in Gilbert syndrome (GS)) may confer a strong genetic advantage.	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-54
31022310-2	2019	In this analysis, functional variants in solute carrier organic anion transporter family member 1B1 (SLCO1B1), uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1), and breast cancer resistance protein (BCRP) were assessed for effects on letermovir pharmacokinetics (PK) using pooled genetic information from 296 participants in 12 phase 1 studies.	letermovir	242-252	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-158
31022310-5	2019	The UGT1A1*6 variant rs4148323 A allele was present predominantly in Asian participants and was associated with an increase in letermovir AUC compared with noncarriers (GMR, 1.36; 95%CI, 1.	letermovir	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
31872743-9	2019	The results of two experiments showed that apigenin was the substrate of UGT1 A1 enzyme,which could inhibit the activity of UGT1 A1 enzyme competitively,and there was a risk of drug interaction between apigenin and UGT1 A1 enzyme substrate in clinical use.	Apigenin	43-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-80
31872743-1	2019	The purpose of this study was to investigate the effect of apigenin on UGT1 A1 enzyme activity and to predict the potential drug-drug interaction of apigenin in clinical use.	Apigenin	59-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-78
31872743-2	2019	First,on the basis of previous experiments,the binding targets and binding strength of apigenin to UGT1 A1 enzyme were predicted by computer molecular docking method.	Apigenin	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-106
31872743-9	2019	The results of two experiments showed that apigenin was the substrate of UGT1 A1 enzyme,which could inhibit the activity of UGT1 A1 enzyme competitively,and there was a risk of drug interaction between apigenin and UGT1 A1 enzyme substrate in clinical use.	Apigenin	43-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-131
31872743-9	2019	The results of two experiments showed that apigenin was the substrate of UGT1 A1 enzyme,which could inhibit the activity of UGT1 A1 enzyme competitively,and there was a risk of drug interaction between apigenin and UGT1 A1 enzyme substrate in clinical use.	Apigenin	43-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-131
31339084-0	2021	UGT1A1 mutations and psychoses: towards understanding the relationship with unconjugated bilirubin.	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
31872743-9	2019	The results of two experiments showed that apigenin was the substrate of UGT1 A1 enzyme,which could inhibit the activity of UGT1 A1 enzyme competitively,and there was a risk of drug interaction between apigenin and UGT1 A1 enzyme substrate in clinical use.	Apigenin	202-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-80
31872743-3	2019	Then the inhibitory effect of apigenin on UGT1 A1 enzyme was evaluated by in vitro human liver microsomal incubation system.	Apigenin	30-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-49
31872743-4	2019	Molecular docking results showed that apigenin was docked into the active region of UGT1 A1 enzyme protein F,consistent with the active region of bilirubin docking,with moderate affinity.	Apigenin	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-91
31872743-4	2019	Molecular docking results showed that apigenin was docked into the active region of UGT1 A1 enzyme protein F,consistent with the active region of bilirubin docking,with moderate affinity.	Bilirubin	146-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-91
31872743-7	2019	These results suggested that the flavonoid mother nucleus structure had a special structure binding to the enzyme protein UGT1 A1,and the introduction of hydroxyl groups into the mother nucleus can increase the binding ability.	Flavonoids	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
31872743-7	2019	These results suggested that the flavonoid mother nucleus structure had a special structure binding to the enzyme protein UGT1 A1,and the introduction of hydroxyl groups into the mother nucleus can increase the binding ability.	Hydroxyl Radical	154-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
31872743-8	2019	In vitro inhibition experiments showed that apigenin had a moderate inhibitory effect on UGT1 A1 enzyme in a way of competitive inhibition,which was consistent with the results of molecular docking.	Apigenin	44-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-96
30820844-8	2019	UGT1A1, 1A3, 1A6, 1A8, 1A9 and 1A10 participated in the formation of D-luciferin glucuronide, with UGT1A1 exhibiting the highest catalytic activity.	d-luciferin glucuronide	69-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
30820844-8	2019	UGT1A1, 1A3, 1A6, 1A8, 1A9 and 1A10 participated in the formation of D-luciferin glucuronide, with UGT1A1 exhibiting the highest catalytic activity.	d-luciferin glucuronide	69-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
30820844-9	2019	Both chemical inhibition assays and kinetic analysis showed that UGT1A1 and UGT1A3 played important roles in D-luciferin-6"-O-glucuronidation in HLM and HIM, with UGT1A6 also giving a non-negligible contribution to this biotransformation in HLM.	D-luciferin	109-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30820844-9	2019	Both chemical inhibition assays and kinetic analysis showed that UGT1A1 and UGT1A3 played important roles in D-luciferin-6"-O-glucuronidation in HLM and HIM, with UGT1A6 also giving a non-negligible contribution to this biotransformation in HLM.	6"-o	121-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30820844-10	2019	CONCLUSIONS: UGT1A1, UGT1A3 and UGT1A6 were responsible for 6"-O-glucuronidation of D-luciferin in HLM, while UGT1A1 and UGT1A3 were the major contributors to this biotransformation in HIM.	6"-o	60-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
30820844-10	2019	CONCLUSIONS: UGT1A1, UGT1A3 and UGT1A6 were responsible for 6"-O-glucuronidation of D-luciferin in HLM, while UGT1A1 and UGT1A3 were the major contributors to this biotransformation in HIM.	D-luciferin	84-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
31175220-1	2019	Cabotegravir, a novel integrase inhibitor under development for treatment and prevention of HIV, is primarily metabolized by UDP-glucuronosyltransferase (UGT)1A1 and UGT1A9 to a direct ether glucuronide metabolite.	cabotegravir	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-161
31175220-1	2019	Cabotegravir, a novel integrase inhibitor under development for treatment and prevention of HIV, is primarily metabolized by UDP-glucuronosyltransferase (UGT)1A1 and UGT1A9 to a direct ether glucuronide metabolite.	ether glucuronide	185-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-161
31207142-6	2019	The family based evaluation of the variants showed that the variant, c.714T > G (p.Tyr238Ter), in the CLEC7A gene in first family; the variant, c.55C > T (p.Arg19Ter), in the APOC3 gene and the variant, c.1171C > T (p.Gln391Ter), in the MUTYH gene in second family; and the variant, c.211G > A (p.Gly71Arg), in the UGT1A1 gene in the third family, were found statistically significant (p < 0.05).	arg19ter	157-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	315-321
30968312-9	2019	For illustration purpose, the approaches were also applied to an irinotecan mixture model demonstrating 36% lower clearance of irinotecan metabolite (SN-38) in individuals with UGT1A1 homo/heterozygote versus wild-type genotype.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
30603911-0	2019	Association between UGT1A1 gene polymorphism and safety and efficacy of irinotecan monotherapy as the third-line treatment for advanced gastric cancer.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
30603911-1	2019	BACKGROUND: While uridine diphosphate glucuronosyltransferase (UGT) 1A1 is a key enzyme in the metabolism of irinotecan, relationship between UGT1A1 genotype and safety and efficacy of irinotecan monotherapy in patients with advanced gastric cancer is not clarified.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-71
30603911-1	2019	BACKGROUND: While uridine diphosphate glucuronosyltransferase (UGT) 1A1 is a key enzyme in the metabolism of irinotecan, relationship between UGT1A1 genotype and safety and efficacy of irinotecan monotherapy in patients with advanced gastric cancer is not clarified.	Irinotecan	185-195	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
30603911-8	2019	CONCLUSIONS: The UGT1A1 polymorphism may be related to the clinical outcomes of irinotecan monotherapy as the third-line treatment for advanced gastric cancer.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
31017737-7	2019	Among the 178 patients of Gilbert"s syndrome, serum bilirubin value was inversely correlated with UGT1A1 activity (r = -.306, P &lt; .001).	Bilirubin	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
31017737-9	2019	Our results demonstrate that UGT1A1 activity is certainly a determinate for serum bilirubin value and UGT1A1 activity  40% of normal is a proper risk factor for the development of Gilbert"s syndrome.	Bilirubin	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
31217818-0	2019	An expansion study of genotype-driven weekly irinotecan and capecitabine in combination with neoadjuvant radiotherapy for locally advanced rectal cancer with UGT1A1 *1*1 genotype.	Irinotecan	45-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
31217818-0	2019	An expansion study of genotype-driven weekly irinotecan and capecitabine in combination with neoadjuvant radiotherapy for locally advanced rectal cancer with UGT1A1 *1*1 genotype.	Capecitabine	60-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
31217818-1	2019	Background: In our previous dose-escalation study, we uncovered the maximum tolerated dose (MTD) of weekly irinotecan was escalated to 80 mg/m2 and 65 mg/m2 for UDP glucuronosyltransferase family 1 member A1 (UGT1A1) *1*1 and *1*28 rectal cancer patients in neoadjuvant chemoradiotherapy (nCRT).	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-207
31217818-1	2019	Background: In our previous dose-escalation study, we uncovered the maximum tolerated dose (MTD) of weekly irinotecan was escalated to 80 mg/m2 and 65 mg/m2 for UDP glucuronosyltransferase family 1 member A1 (UGT1A1) *1*1 and *1*28 rectal cancer patients in neoadjuvant chemoradiotherapy (nCRT).	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
30968312-9	2019	For illustration purpose, the approaches were also applied to an irinotecan mixture model demonstrating 36% lower clearance of irinotecan metabolite (SN-38) in individuals with UGT1A1 homo/heterozygote versus wild-type genotype.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
30968312-9	2019	For illustration purpose, the approaches were also applied to an irinotecan mixture model demonstrating 36% lower clearance of irinotecan metabolite (SN-38) in individuals with UGT1A1 homo/heterozygote versus wild-type genotype.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
31150474-0	2019	Mechanism of the efflux transport of demethoxycurcumin-O-glucuronides in HeLa cells stably transfected with UDP-glucuronosyltransferase 1A1.	demethoxycurcumin-o-glucuronides	37-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-139
30044687-7	2019	UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9, UGT1A10 and UGT2B7 participated in the formation of 4-O-glucuronide, with UGT1A9 exhibiting the highest catalytic activity in this biotransformation.	4-o-glucuronide	92-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
30044687-8	2019	Only UGT1A1 and UGT1A3 were involved in the formation of 4"-O-glucuronide, exhibiting similar reaction rates.	4"-o-glucuronide	57-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
30044687-10	2019	UGT1A9 was the major contributor to the formation of LCA-4-O-glucuronide, while UGT1A1 played important roles in both LCA-4-O- and 4"-O-glucuronidation.	4"-o	131-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
31150474-3	2019	In this study, we aimed to investigate the formation of DMC-O-glucuronides by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and its transport by breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins (MRPs) in HeLa cells stably transfected with UGT1A1 (named HeLa1A1 cells).	dmc-o-glucuronides	56-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-126
31150474-3	2019	In this study, we aimed to investigate the formation of DMC-O-glucuronides by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and its transport by breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins (MRPs) in HeLa cells stably transfected with UGT1A1 (named HeLa1A1 cells).	dmc-o-glucuronides	56-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	287-293
31150474-3	2019	In this study, we aimed to investigate the formation of DMC-O-glucuronides by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and its transport by breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins (MRPs) in HeLa cells stably transfected with UGT1A1 (named HeLa1A1 cells).	dmc-o-glucuronides	56-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
30645764-0	2019	A UGT1A1 genotype-guided dosing study of modified FOLFIRINOX in previously untreated patients with advanced gastrointestinal malignancies.	folfirinox	50-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	2-8
31142299-2	2019	CNs type II patients usually benefit from phenobarbital treatment that induces residual UGT1A1 activity.	Phenobarbital	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
30645764-2	2019	UGT1A1 (UDP glucuronosyltransferase 1A1) eliminates the active metabolite of irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
30645764-2	2019	UGT1A1 (UDP glucuronosyltransferase 1A1) eliminates the active metabolite of irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
30645764-4	2019	The primary objective was to determine the dose-limiting toxicity (DLT) rate in cycle 1 of modified FOLFIRINOX (mFOLFIRINOX) using genotype-guided dosing of irinotecan for the most common UGT1A1 genotypes (*1/*1, *1/*28) in advanced gastrointestinal malignancies, with expansion in pancreatic and biliary tract cancers.	folfirinox	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
30645764-4	2019	The primary objective was to determine the dose-limiting toxicity (DLT) rate in cycle 1 of modified FOLFIRINOX (mFOLFIRINOX) using genotype-guided dosing of irinotecan for the most common UGT1A1 genotypes (*1/*1, *1/*28) in advanced gastrointestinal malignancies, with expansion in pancreatic and biliary tract cancers.	mfolfirinox	112-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
30645764-6	2019	Irinotecan doses of 180, 135, and 90 mg/m2 were administered for UGT1A1 genotypes *1/*1, *1/*28, and *28/*28, respectively.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30645764-13	2019	CONCLUSION: On the basis of our prespecified criteria, tolerability of UGT1A1 genotype-guided mFOLFIRINOX was not established in pancreatic and biliary tract cancers.	mfolfirinox	94-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
30810774-6	2019	RESULTS: Concentration-dependent inhibition of SN-38 glucuronidation was observed in the HLMs and recombinant human UGT1A1 experiments: Pazopanib noncompetitively inhibited SN-38 glucuronidation by HLMs (Ki,u = 1.6 +- 0.05 microM) and recombinant human UGT1A1 (Ki,u = 0.69 +- 0.02 microM).	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
30962262-0	2019	Association between the UGT1A1*28 allele and hyperbilirubinemia in HIV-positive patients receiving atazanavir: a meta-analysis.	Atazanavir Sulfate	99-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
30962262-1	2019	Objectives The uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1)*28 allele in HIV-positive patients receiving atazanavir (ATV) might be associated with the risk of hyperbilirubinemia.	Atazanavir Sulfate	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-62
30962262-1	2019	Objectives The uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1)*28 allele in HIV-positive patients receiving atazanavir (ATV) might be associated with the risk of hyperbilirubinemia.	Atazanavir Sulfate	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
30962262-1	2019	Objectives The uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1)*28 allele in HIV-positive patients receiving atazanavir (ATV) might be associated with the risk of hyperbilirubinemia.	Atazanavir Sulfate	129-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-62
30962262-1	2019	Objectives The uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1)*28 allele in HIV-positive patients receiving atazanavir (ATV) might be associated with the risk of hyperbilirubinemia.	Atazanavir Sulfate	129-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
30962262-7	2019	A significantly increased risk of hyperbilirubinemia was observed in HIV-positive patients receiving ATV with the UGT1A1*1/*28 or UGT1A1*28/*28 genotype, and the risk was higher with the UGT1A1*28/*28 genotype than with the UGT1A1*1/*28 genotype.	Atazanavir Sulfate	101-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
30962262-7	2019	A significantly increased risk of hyperbilirubinemia was observed in HIV-positive patients receiving ATV with the UGT1A1*1/*28 or UGT1A1*28/*28 genotype, and the risk was higher with the UGT1A1*28/*28 genotype than with the UGT1A1*1/*28 genotype.	Atazanavir Sulfate	101-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
30962262-7	2019	A significantly increased risk of hyperbilirubinemia was observed in HIV-positive patients receiving ATV with the UGT1A1*1/*28 or UGT1A1*28/*28 genotype, and the risk was higher with the UGT1A1*28/*28 genotype than with the UGT1A1*1/*28 genotype.	Atazanavir Sulfate	101-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
30962262-7	2019	A significantly increased risk of hyperbilirubinemia was observed in HIV-positive patients receiving ATV with the UGT1A1*1/*28 or UGT1A1*28/*28 genotype, and the risk was higher with the UGT1A1*28/*28 genotype than with the UGT1A1*1/*28 genotype.	Atazanavir Sulfate	101-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
30962262-9	2019	All of the pooled ORs were not significantly affected by the remaining studies and different modeling methods, indicating robust results.Conclusions This meta-analysis suggests that the UGT1A1*28 allele represents a biomarker for an increased risk of hyperbilirubinemia in HIV-positive patients receiving ATV.	Atazanavir Sulfate	305-308	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-192
30589990-4	2019	Studies verified predisposition of HIV-positive carriers of UGT1A1*28 to severe atazanavir-induced hyperbilirubinaemia, intolerance to 5-fluorouracyl in gastrointestinal cancer patients with deleterious DPYD variants, failure of HCV-infected carriers of IFNL3 rs12979860 to obtain a sustained viral response to PEG-IFN-alpha, and hypersensitivity reactions to abacavir in HIV-positive carriers of HLA-B*57:01.	Atazanavir Sulfate	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
30589990-4	2019	Studies verified predisposition of HIV-positive carriers of UGT1A1*28 to severe atazanavir-induced hyperbilirubinaemia, intolerance to 5-fluorouracyl in gastrointestinal cancer patients with deleterious DPYD variants, failure of HCV-infected carriers of IFNL3 rs12979860 to obtain a sustained viral response to PEG-IFN-alpha, and hypersensitivity reactions to abacavir in HIV-positive carriers of HLA-B*57:01.	5-fluorouracyl	135-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
30589990-4	2019	Studies verified predisposition of HIV-positive carriers of UGT1A1*28 to severe atazanavir-induced hyperbilirubinaemia, intolerance to 5-fluorouracyl in gastrointestinal cancer patients with deleterious DPYD variants, failure of HCV-infected carriers of IFNL3 rs12979860 to obtain a sustained viral response to PEG-IFN-alpha, and hypersensitivity reactions to abacavir in HIV-positive carriers of HLA-B*57:01.	peg-ifn-alpha	311-324	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
30589990-4	2019	Studies verified predisposition of HIV-positive carriers of UGT1A1*28 to severe atazanavir-induced hyperbilirubinaemia, intolerance to 5-fluorouracyl in gastrointestinal cancer patients with deleterious DPYD variants, failure of HCV-infected carriers of IFNL3 rs12979860 to obtain a sustained viral response to PEG-IFN-alpha, and hypersensitivity reactions to abacavir in HIV-positive carriers of HLA-B*57:01.	abacavir	360-368	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
30810774-0	2019	Pazopanib interacts with irinotecan by inhibiting UGT1A1-mediated glucuronidation, but not OATP1B1-mediated hepatic uptake, of an active metabolite SN-38.	pazopanib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
30810774-0	2019	Pazopanib interacts with irinotecan by inhibiting UGT1A1-mediated glucuronidation, but not OATP1B1-mediated hepatic uptake, of an active metabolite SN-38.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
30810774-3	2019	To clarify the possible mechanism underlying that drug-drug interaction, we investigated the potential for pazopanib to inhibit UDP-glucuronosyltransferase (UGT)1A1 and organic anion-transporting polypeptide (OATP)1B1, which are involved in detoxification and hepatic uptake of SN-38, respectively.	pazopanib	107-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-164
30810774-6	2019	RESULTS: Concentration-dependent inhibition of SN-38 glucuronidation was observed in the HLMs and recombinant human UGT1A1 experiments: Pazopanib noncompetitively inhibited SN-38 glucuronidation by HLMs (Ki,u = 1.6 +- 0.05 microM) and recombinant human UGT1A1 (Ki,u = 0.69 +- 0.02 microM).	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	253-259
30810774-6	2019	RESULTS: Concentration-dependent inhibition of SN-38 glucuronidation was observed in the HLMs and recombinant human UGT1A1 experiments: Pazopanib noncompetitively inhibited SN-38 glucuronidation by HLMs (Ki,u = 1.6 +- 0.05 microM) and recombinant human UGT1A1 (Ki,u = 0.69 +- 0.02 microM).	pazopanib	136-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
30810774-6	2019	RESULTS: Concentration-dependent inhibition of SN-38 glucuronidation was observed in the HLMs and recombinant human UGT1A1 experiments: Pazopanib noncompetitively inhibited SN-38 glucuronidation by HLMs (Ki,u = 1.6 +- 0.05 microM) and recombinant human UGT1A1 (Ki,u = 0.69 +- 0.02 microM).	pazopanib	136-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	253-259
30810774-10	2019	CONCLUSIONS: Results showed that pazopanib inhibits UGT1A1-mediated SN-38 glucuronidation, but not OATP1B1-mediated SN-38 uptake.	pazopanib	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
30810774-10	2019	CONCLUSIONS: Results showed that pazopanib inhibits UGT1A1-mediated SN-38 glucuronidation, but not OATP1B1-mediated SN-38 uptake.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
30804050-7	2019	The kinetic data from expression systems suggested the major enzymes in each tissue: hepatic UGT1A9 &gt; UGT1A1 (dolutegravir and raltegravir) and UGT1A1 (cabotegravir), intestinal UGT1A3 &gt; UGT1A8 &gt; UGT1A1 (dolutegravir) and UGT1A8 &gt; UGT1A1 (raltegravir), and renal UGT1A9 (dolutegravir and raltegravir).	dolutegravir	113-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
30804050-7	2019	The kinetic data from expression systems suggested the major enzymes in each tissue: hepatic UGT1A9 &gt; UGT1A1 (dolutegravir and raltegravir) and UGT1A1 (cabotegravir), intestinal UGT1A3 &gt; UGT1A8 &gt; UGT1A1 (dolutegravir) and UGT1A8 &gt; UGT1A1 (raltegravir), and renal UGT1A9 (dolutegravir and raltegravir).	cabotegravir	155-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
30804050-7	2019	The kinetic data from expression systems suggested the major enzymes in each tissue: hepatic UGT1A9 &gt; UGT1A1 (dolutegravir and raltegravir) and UGT1A1 (cabotegravir), intestinal UGT1A3 &gt; UGT1A8 &gt; UGT1A1 (dolutegravir) and UGT1A8 &gt; UGT1A1 (raltegravir), and renal UGT1A9 (dolutegravir and raltegravir).	cabotegravir	155-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
30804050-7	2019	The kinetic data from expression systems suggested the major enzymes in each tissue: hepatic UGT1A9 &gt; UGT1A1 (dolutegravir and raltegravir) and UGT1A1 (cabotegravir), intestinal UGT1A3 &gt; UGT1A8 &gt; UGT1A1 (dolutegravir) and UGT1A8 &gt; UGT1A1 (raltegravir), and renal UGT1A9 (dolutegravir and raltegravir).	cabotegravir	155-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
31164525-0	2019	[FOLFIRINOX for Locally Advanced and Recurrent Pancreatic Cancer with UGT1A1 *6 and or UGT1A1*28 Polymorphisms-A Report of Two Cases].	folfirinox	1-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
30339275-7	2019	In patients receiving fluoropyrimidine/irinotecan, the incremental cost between DPYD variant and UGT1A1*28/*28 carriers and noncarriers was $2,975.	2-fluoropyrimidine	22-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
30339275-7	2019	In patients receiving fluoropyrimidine/irinotecan, the incremental cost between DPYD variant and UGT1A1*28/*28 carriers and noncarriers was $2,975.	Irinotecan	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
30339275-8	2019	This study suggests that the toxicity management costs during fluoropyrimidine-based therapy are associated with DPYD and UGT1A1*28 variants and supports the utility of genotyping.	2-fluoropyrimidine	62-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
31069991-4	2019	Hyperbilirubinemia can also be caused by impaired bilirubin conjugation due to polymorphisms and mutations in genes involved in bilirubin metabolism (eg, UGT1A1).	Bilirubin	5-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
31069991-4	2019	Hyperbilirubinemia can also be caused by impaired bilirubin conjugation due to polymorphisms and mutations in genes involved in bilirubin metabolism (eg, UGT1A1).	Bilirubin	50-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
30583998-8	2019	Patients treated with aspirin were significantly more common in the UGT1A1*28/*28 homozygous group than in the other groups (7/23 (30.4%) compared to 22/269 (8.2%), p = 0.001).	Aspirin	22-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
30583998-9	2019	CONCLUSION: Dinucleotide polymorphism in the promoter region of the UGT1A1 gene is not associated with a specific colonic phenotype in patients with sporadic colorectal cancer.	Dinucleoside Phosphates	12-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
31164525-0	2019	[FOLFIRINOX for Locally Advanced and Recurrent Pancreatic Cancer with UGT1A1 *6 and or UGT1A1*28 Polymorphisms-A Report of Two Cases].	folfirinox	1-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
30594625-0	2019	Inhibition of UGT1A1 by natural and synthetic flavonoids.	Flavonoids	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	folfirinox	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
30594625-2	2019	Recent studies demonstrate that some natural flavonoids are potent inhibitors of the human UDP-glucuronosyltransferase 1A1 (UGT1A1), a key enzyme in detoxification of endogenous harmful compounds such as bilirubin.	Flavonoids	45-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-122
30594625-5	2019	Further investigation on inhibition kinetics of two strong flavonoid-type UGT1A1 inhibitors, acacetin and kaempferol, yielded interesting results.	kaempferol	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
31164525-6	2019	Since the determined regimen of FOLFIRINOX for patients with high-risk UGT1A1 polymorphisms has not been developed yet, it would be critical to accumulate and review an experience of FOLFIRINOX administration for these patients.	folfirinox	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
30594625-6	2019	Both flavonoids were competitive inhibitors against UGT1A1-mediated NHPN-O-glucuronidation, but were mixed and competitive inhibitors toward UGT1A1-mediated NCHN-O-glucuronidation, respectively.	Flavonoids	5-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
30594625-2	2019	Recent studies demonstrate that some natural flavonoids are potent inhibitors of the human UDP-glucuronosyltransferase 1A1 (UGT1A1), a key enzyme in detoxification of endogenous harmful compounds such as bilirubin.	Flavonoids	45-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
30594625-2	2019	Recent studies demonstrate that some natural flavonoids are potent inhibitors of the human UDP-glucuronosyltransferase 1A1 (UGT1A1), a key enzyme in detoxification of endogenous harmful compounds such as bilirubin.	Bilirubin	204-213	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-122
31164525-6	2019	Since the determined regimen of FOLFIRINOX for patients with high-risk UGT1A1 polymorphisms has not been developed yet, it would be critical to accumulate and review an experience of FOLFIRINOX administration for these patients.	folfirinox	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
30594625-2	2019	Recent studies demonstrate that some natural flavonoids are potent inhibitors of the human UDP-glucuronosyltransferase 1A1 (UGT1A1), a key enzyme in detoxification of endogenous harmful compounds such as bilirubin.	Bilirubin	204-213	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
30594625-3	2019	In this study, the inhibitory effects of 56 natural and synthetic flavonoids on UGT1A1 were assayed, while the structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated.	Flavonoids	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
30594625-4	2019	The results demonstrated that the C-3 and C-7 hydroxyl groups on the flavone skeleton would enhance UGT1A1 inhibition, while flavonoid glycosides displayed weaker inhibitory effects than their corresponding aglycones.	flavone	69-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
30594625-5	2019	Further investigation on inhibition kinetics of two strong flavonoid-type UGT1A1 inhibitors, acacetin and kaempferol, yielded interesting results.	Flavonoids	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
30594625-5	2019	Further investigation on inhibition kinetics of two strong flavonoid-type UGT1A1 inhibitors, acacetin and kaempferol, yielded interesting results.	acacetin	93-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
30594625-6	2019	Both flavonoids were competitive inhibitors against UGT1A1-mediated NHPN-O-glucuronidation, but were mixed and competitive inhibitors toward UGT1A1-mediated NCHN-O-glucuronidation, respectively.	Flavonoids	5-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
29543105-7	2019	UGT1A6 and UGT1A1 played a major role in R/S-6- and 7-hydroxywarfarin glucuronidation, respectively, whereas UGT1A9 accounted for almost all of the generation of the R/S-8-hydroxywarfarin glucuronide.	r	41-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
30594625-6	2019	Both flavonoids were competitive inhibitors against UGT1A1-mediated NHPN-O-glucuronidation, but were mixed and competitive inhibitors toward UGT1A1-mediated NCHN-O-glucuronidation, respectively.	nchn-o	157-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	kaempferol	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	acacetin	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	acacetin	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	Bilirubin	172-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	Bilirubin	172-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
30594625-8	2019	In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.	Flavonoids	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
30736072-8	2019	Glucuronidation of isoscopoletin and scopoletin was catalyzed by the human UGT1A1, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, and UGT2B17.	isoscopoletin	19-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
30736072-8	2019	Glucuronidation of isoscopoletin and scopoletin was catalyzed by the human UGT1A1, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, and UGT2B17.	Scopoletin	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
29543105-7	2019	UGT1A6 and UGT1A1 played a major role in R/S-6- and 7-hydroxywarfarin glucuronidation, respectively, whereas UGT1A9 accounted for almost all of the generation of the R/S-8-hydroxywarfarin glucuronide.	s-6- and 7-hydroxywarfarin	43-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
30919115-7	2019	The median dose of lenvatinib in patients with UGT1A1*6/*6 or *6/*28 (poor metabolizers [PMs]) was significantly lower than that in patients with UGT1A1*1/*1 (10 and 14 mg, respectively), whereas the median bilirubin levels were significant higher in UGT1A1 PMs (0.9 and 0.5 mg/dL, respectively).	lenvatinib	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
30328531-0	2019	Influence of UGT1A1 polymorphism on etoposide plus platinum-induced neutropenia in Japanese patients with small-cell lung cancer.	Etoposide	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
30328531-9	2019	CONCLUSIONS: UGT1A1*28 and UGT1A1*6 mutations might be regarded as predictors for etoposide-induced grade 4 neutropenia.	Etoposide	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
30328531-0	2019	Influence of UGT1A1 polymorphism on etoposide plus platinum-induced neutropenia in Japanese patients with small-cell lung cancer.	Platinum	51-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
30328531-1	2019	BACKGROUND: The association between UGT1A1 polymorphism and etoposide-induced toxicities is still not clear.	Etoposide	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
30328531-2	2019	The aim of this study was to assess the association between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphism and severe hematologic toxicities in Japanese patients receiving etoposide plus platinum chemotherapy for small-cell lung cancer.	Etoposide	200-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-107
30328531-2	2019	The aim of this study was to assess the association between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphism and severe hematologic toxicities in Japanese patients receiving etoposide plus platinum chemotherapy for small-cell lung cancer.	Etoposide	200-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
30328531-2	2019	The aim of this study was to assess the association between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphism and severe hematologic toxicities in Japanese patients receiving etoposide plus platinum chemotherapy for small-cell lung cancer.	Platinum	215-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-107
30328531-2	2019	The aim of this study was to assess the association between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphism and severe hematologic toxicities in Japanese patients receiving etoposide plus platinum chemotherapy for small-cell lung cancer.	Platinum	215-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
30328531-6	2019	The incidence of grade 4 neutropenia during the first cycle of etoposide-based chemotherapy was higher in patients with homozygous (hmz) polymorphisms for UGT1A1*28 and *6 (*28/*28, *6/*6, and *6/*28) than in patients with wild-type (wt) (*1/*1) and heterozygous (htz) (*1/*28 and *1/*6) polymorphisms (88% vs 43% P = 0.03).	Etoposide	63-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
30328531-9	2019	CONCLUSIONS: UGT1A1*28 and UGT1A1*6 mutations might be regarded as predictors for etoposide-induced grade 4 neutropenia.	Etoposide	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
30820183-7	2019	Pretreatment levels of ferritin and bilirubin were associated with the presence of UGT1A1*28 genotype, indicating its potential as a predictive marker.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
30628534-0	2019	Cost-effectiveness analysis of UGT1A1*6/*28 genotyping for preventing FOLFIRI-induced severe neutropenia in Chinese colorectal cancer patients.	FOLFIRI regimen	70-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
29436891-8	2019	Glucuronidation of alpinetin was significantly correlated with glucuronidation of estradiol (an activity marker of UGT1A1), chenodeoxycholic acid (an activity marker of UGT1A3), propofol (an activity marker of UGT1A9) and 5-hydroxyrofecoxib (an activity marker of UGT2B15), confirming the important roles of UGT1A1, UGT1A3, UGT1A9 and UGT2B15 in alpinetin glucuronidation.	alpinetin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
30466000-6	2019	Moreover, RA weakly inhibited CYP2C9 and 2E1 activities with IC50 values of 39.6 and 61.0 muM, respectively, while moderately inhibiting UGT1A1, 1A6, and 2B7 with IC50 values of 9.24, 19.1, and 23.4 muM, respectively.	rosmarinic acid	10-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
29436891-8	2019	Glucuronidation of alpinetin was significantly correlated with glucuronidation of estradiol (an activity marker of UGT1A1), chenodeoxycholic acid (an activity marker of UGT1A3), propofol (an activity marker of UGT1A9) and 5-hydroxyrofecoxib (an activity marker of UGT2B15), confirming the important roles of UGT1A1, UGT1A3, UGT1A9 and UGT2B15 in alpinetin glucuronidation.	alpinetin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	308-314
29436891-8	2019	Glucuronidation of alpinetin was significantly correlated with glucuronidation of estradiol (an activity marker of UGT1A1), chenodeoxycholic acid (an activity marker of UGT1A3), propofol (an activity marker of UGT1A9) and 5-hydroxyrofecoxib (an activity marker of UGT2B15), confirming the important roles of UGT1A1, UGT1A3, UGT1A9 and UGT2B15 in alpinetin glucuronidation.	Estradiol	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
31633039-3	2019	Pharmacogenetics is increasingly used to stratify patients for precision medicine treatments, for instance, the UGT1A1*28 polymorphism as a dosage indicator for the use of irinotecan as well as epidermal growth factor receptor (EGFR) immunohistochemistry and KRAS Proto-Oncogene (KRAS) exon 2 mutation tests for determining the likelihood of treatment response to cetuximab or panitumumab treatment in metastatic colorectal cancer (CRC).	irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
30466000-2	2019	The involvement of selected enzymes (CYP1A2, CYP2C19, CYP2E1, CYP3 A4, UGT1A1, UGT1A6, and UGT2B7) in the metabolism of RA and the inhibitory effect of RA on the enzyme activity were comprehensively evaluated using human recombinant isozyme system.	rosmarinic acid	120-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
30466000-7	2019	By constructing Line weaver-Burk plots, the type of inhibition exhibited by RA on CYP and UGT activities was determined as follows: CYP2C19, mixed inhibition; CYP2E1, UGT1A1, UGT1A6, and UGT2B7, competitive inhibition.	rosmarinic acid	76-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
30447099-0	2019	Impact of UGT1A1 genetic polymorphism on toxicity in unresectable pancreatic cancer patients undergoing FOLFIRINOX.	folfirinox	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
30447099-1	2019	Studies have indicated an association between UDP-glucuronosyltransferase-1A1 (UGT1A1) genetic polymorphisms and irinotecan-induced toxicity.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-77
30447099-1	2019	Studies have indicated an association between UDP-glucuronosyltransferase-1A1 (UGT1A1) genetic polymorphisms and irinotecan-induced toxicity.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
31685767-0	2019	Study on the Optimal Dose of Irinotecan for Patients with Heterozygous Uridine Diphosphate-Glucuronosyltransferase 1A1 (UGT1A1).	irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-118
30447099-2	2019	We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study.	folfirinox	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
30447099-2	2019	We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study.	Oxaliplatin	157-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
30447099-2	2019	We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study.	Irinotecan	170-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
30447099-2	2019	We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study.	Fluorouracil	182-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
30447099-2	2019	We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study.	Leucovorin	200-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
30447099-7	2019	In the original FOLFIRINOX group, the incidence of diarrhea was significantly higher among patients with UGT1A1 heterozygous type than among those with UGT1A1 WT and the incidence of leukopenia and diarrhea was significantly higher among patients with UGT1A1 -/*6 than among those with UGT1A1 -/*28.	folfirinox	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
30447099-7	2019	In the original FOLFIRINOX group, the incidence of diarrhea was significantly higher among patients with UGT1A1 heterozygous type than among those with UGT1A1 WT and the incidence of leukopenia and diarrhea was significantly higher among patients with UGT1A1 -/*6 than among those with UGT1A1 -/*28.	folfirinox	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
30447099-7	2019	In the original FOLFIRINOX group, the incidence of diarrhea was significantly higher among patients with UGT1A1 heterozygous type than among those with UGT1A1 WT and the incidence of leukopenia and diarrhea was significantly higher among patients with UGT1A1 -/*6 than among those with UGT1A1 -/*28.	folfirinox	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
30447099-7	2019	In the original FOLFIRINOX group, the incidence of diarrhea was significantly higher among patients with UGT1A1 heterozygous type than among those with UGT1A1 WT and the incidence of leukopenia and diarrhea was significantly higher among patients with UGT1A1 -/*6 than among those with UGT1A1 -/*28.	folfirinox	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
30447099-10	2019	In conclusion, patients with heterozygous UGT1A1 polymorphisms treated with the original FOLFIRINOX regimen experienced severe toxicity more frequently than patients with WT UGT1A1.	folfirinox	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
30439556-6	2019	Butyrate also promoted induction of CYP1, NQO1, NAT2, UGT1A1 or UGT1A4 in human colon Caco-2 cells, in a differentiation-dependent manner.	Butyrates	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
30439556-10	2019	In some cases (NAT2, UGT1 A1), this was linked to inhibition of histone deacetylases (HDAC), as confirmed by using HDAC inhibitor trichostatin A.	trichostatin A	130-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-28
30421550-0	2019	Prolonged central apnoea after intravenous morphine administration in a 12-year-old male with a UGT1A1 loss-of-function polymorphism.	Morphine	43-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
29357726-7	2019	TSI could be reduced to a relatively unstable hydroquinone intermediate by NAD(P)H: quinone oxidoreductase 1 (NQO1), and then immediately conjugated with glucuronic acid by a panel of UGTs, especially UGT1A9, UGT1A1 and UGT1A8.	Glucuronic Acid	154-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
29357726-8	2019	Additionally, NQO1 could also reduce hydroxylated TSI to a hydroquinone intermediate, which was immediately glucuronidated by UGT1A1.	hydroquinone	59-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
30439556-4	2019	In combination with BaP, butyrate potentiated induction of cytochrome P450 family 1 enzymes (CYP1A1), aldo-keto reductases (AKR1C1) or UDP-glucuronosyltransferases (UGT1A1).	Butyrates	25-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
31054979-2	2019	To examine this hypothesis, we investigated the relationship between plasma bilirubin concentrations and bilirubin UDP-glucuronosyl transferase (UGT1A1) promoter gene variations (associated with increased bilirubin concentrations) with total/CVD and cancer mortality.	Bilirubin	76-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
31054979-2	2019	To examine this hypothesis, we investigated the relationship between plasma bilirubin concentrations and bilirubin UDP-glucuronosyl transferase (UGT1A1) promoter gene variations (associated with increased bilirubin concentrations) with total/CVD and cancer mortality.	Bilirubin	105-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
31054979-2	2019	To examine this hypothesis, we investigated the relationship between plasma bilirubin concentrations and bilirubin UDP-glucuronosyl transferase (UGT1A1) promoter gene variations (associated with increased bilirubin concentrations) with total/CVD and cancer mortality.	Bilirubin	105-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
31054979-10	2019	The UGT1A1*28 allele, a genetic marker of raised bilirubin, was also negatively associated with total/cancer mortality, although the associations were not statistically significant.	Bilirubin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
30585257-1	2019	BACKGROUND: Patients harbouring the UGT1A1*28/*28 genotype are at risk of severe toxicity with the standard irinotecan dose.	Irinotecan	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
30585257-6	2019	In the experimental group, the irinotecan dose was 300 mg/m2 for UGT1A1*1/*1 and 260 mg/m2 for *1/*28 patients.	Irinotecan	31-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30585257-13	2019	CONCLUSIONS: Patients with the UGT1A1*1/*1 and *1/*28 genotypes can receive high doses of irinotecan to achieve a more favourable ORR without significant adverse events.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
31685767-0	2019	Study on the Optimal Dose of Irinotecan for Patients with Heterozygous Uridine Diphosphate-Glucuronosyltransferase 1A1 (UGT1A1).	irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
31685767-1	2019	Uridine 5"-diphospho-glucuronosyltransferase (UGT), a metabolic enzyme of irinotecan active metabolite, has two genetic polymorphisms (UGT1A1*6 and UGT1A1*28).	irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
31685767-1	2019	Uridine 5"-diphospho-glucuronosyltransferase (UGT), a metabolic enzyme of irinotecan active metabolite, has two genetic polymorphisms (UGT1A1*6 and UGT1A1*28).	irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
30421550-4	2019	EVIDENCE THAT LINKS DRUG TO EVENT: Pharmacogenomic testing revealed that the patient was homozygous for the T allele at the rs887829 SNP in UGT1A1, an enzyme involved in the metabolism of morphine.	Morphine	188-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
31685767-2	2019	In UGT1A1 homozygous or heterozygous patients, metabolism is delayed and the risk of developing adverse effects is increased, and therefore, dose reduction of irinotecan is considered.	irinotecan	159-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	3-9
30421550-6	2019	MECHANISM: Morphine is metabolized by UDP-glucuronosyltransferase (UGT)-2B7 and UGT1A1 to form its major metabolites morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G).	Morphine	11-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
31685767-11	2019	For lung cancer patients with UGT1A1 heterozygote types who start irinotecan therapy, reducing the initial dose by approximately 20% might be a safer chemotherapy without decreasing the therapeutic effect.	irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
30421550-6	2019	MECHANISM: Morphine is metabolized by UDP-glucuronosyltransferase (UGT)-2B7 and UGT1A1 to form its major metabolites morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G).	morphine-3-glucuronide	117-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
30377777-11	2019	CONCLUSION: The present study demonstrated that dose reduction by 20% ensured safety and efficacy of irinotecan in mCRC patients with homozygous mutation in UGT1A1 genes.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
30421550-6	2019	MECHANISM: Morphine is metabolized by UDP-glucuronosyltransferase (UGT)-2B7 and UGT1A1 to form its major metabolites morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G).	morphine-6-glucuronide	150-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
30421550-7	2019	Our patient was a poor metabolizer through UGT1A1, likely leading to increased respiratory depression as morphine has greater respiratory depressant effects compared to its metabolites.	Morphine	105-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
30377777-0	2019	Dose adjustment of irinotecan based on UGT1A1 polymorphisms in patients with colorectal cancer.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
29932028-4	2019	SN-38 is detoxified by the formation of SN-38 glucuronide, through UGT1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
30377777-2	2019	SN-38 is an active metabolite of irinotecan, which is formed by carboxylesterase and inactivated by UDP-glucuronyltransferase (UGT) 1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-135
30377777-2	2019	SN-38 is an active metabolite of irinotecan, which is formed by carboxylesterase and inactivated by UDP-glucuronyltransferase (UGT) 1A1.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-135
30377777-3	2019	The UGT enzyme activity is reduced in patients with homozygous mutation in UGT1A1 genes (*6/*6, *28/*28 and *6/*28); thus dose reduction is required for prevention of severe adverse events associated with irinotecan.	Irinotecan	205-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
30377777-4	2019	The present study was designed to investigate the relationship between UGT1A1 polymorphisms and the incidence of adverse events or the therapeutic effect in mCRC patients who received irinotecan.	Irinotecan	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
29932028-4	2019	SN-38 is detoxified by the formation of SN-38 glucuronide, through UGT1A1.	7-ethyl-10-hydroxycamptothecin glucuronide	40-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
29932028-5	2019	Genetic polymorphisms in the UGT1A1 gene are associated to higher exposures to SN-38 and severe toxicity.	Irinotecan	79-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
30171692-0	2018	CYP3A4-mediated effects of rifampicin on the pharmacokinetics of vilaprisan and its UGT1A1-mediated effects on bilirubin glucuronidation in humans.	Bilirubin	111-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	98-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	98-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
30619479-9	2018	The variants of UGT1A1 *28 and UGT1A1 *6 were strongly associated with increased total bilirubin (TB), direct bilirubin (DB), and indirect bilirubin (IB) levels (each P &lt; 0.001).	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30385458-4	2019	CN-1 is an autosomal recessive disorder caused by damaging mutations in the gene for UGT1A1, the hepatic enzyme responsible for bilirubin conjugation in humans.	Bilirubin	128-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
30527657-1	2019	Differences in drug metabolism associated with UGT1A1 polymorphism could result in individualized local response to hepatic chemoembolization with irinotecan-eluting beads (DEBIRI) or predictable toxicities.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
30397001-7	2019	Moreover, CCAR1 could be recruited to the gtPBREM of the UGT1A1 enhancer by CAR but not to the PBREM of the CYP2B6 enhancer.	gtpbrem	42-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
30599907-12	2019	CONCLUSION: The results indicated that the HF originated overexpression of Ugt1a1, Ugt1a7, and P-gp level played important roles in pharmacokinetics of puerarin, suggested the clinical regimen of puerarin based on normal populations might be inappropriate for patients with chronic liver diseases.	puerarin	152-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
30599907-12	2019	CONCLUSION: The results indicated that the HF originated overexpression of Ugt1a1, Ugt1a7, and P-gp level played important roles in pharmacokinetics of puerarin, suggested the clinical regimen of puerarin based on normal populations might be inappropriate for patients with chronic liver diseases.	puerarin	196-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
30237061-0	2018	The roles of breast cancer resistance protein (BCRP/ABCG2) and multidrug resistance-associated proteins (MRPs/ABCCs) in the excretion of cycloicaritin-3-O-glucoronide in UGT1A1-overexpressing HeLa cells.	cycloicaritin-3-o-glucoronide	137-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
30237061-4	2018	First, beta-estradiol was used to validate the expression of active UGT1A1 protein in engineered HeLa1A1 cells.	Estradiol	7-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
30237061-9	2018	Meanwhile, the UGT1A1 modified HeLa cells were a simple and practical tool to study UGT1A1-mediated glucuronidation and to characterize BCRP and MRPs-mediated glucuronide transport at a cellular level.	Glucuronides	159-170	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
30171692-2	2018	In addition, the effects of rifampicin on the glucuronidation of bilirubin, an endogenous UDP-glucuronosyltransferase family 1 member A1 (UGT1A1) substrate, were explored.	Bilirubin	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-136
30246377-0	2018	UGT1A1 polymorphisms in rectal cancer associated with the efficacy and toxicity of preoperative chemoradiotherapy using irinotecan.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
30246377-11	2018	Our results indicate that UGT1A1 polymorphism is a predictive factor to determine the clinical efficacy of preoperative chemoradiotherapy and hematological toxicity induced by chemoradiotherapy using irinotecan in locally advanced rectal cancer patients.	Irinotecan	200-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
30171692-2	2018	In addition, the effects of rifampicin on the glucuronidation of bilirubin, an endogenous UDP-glucuronosyltransferase family 1 member A1 (UGT1A1) substrate, were explored.	Bilirubin	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
30246377-1	2018	The purpose of the present study was to assess the efficacy and toxicity of preoperative chemoradiotherapy using irinotecan against locally advanced lower rectal cancer according to UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphisms.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-213
30246377-1	2018	The purpose of the present study was to assess the efficacy and toxicity of preoperative chemoradiotherapy using irinotecan against locally advanced lower rectal cancer according to UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphisms.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	215-221
30171692-10	2018	Further, it was associated with an increase in bilirubin glucuronidation, indicating that UGT1A1 was induced.	Bilirubin	47-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
30105552-6	2018	This study demonstrates that different variations present in the UGT1A1 gene and specifically, the H55R variation had a significant effect on bilirubin levels and could be genetic risk factors for hyperbilirubinemia.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30194276-0	2018	6-Chloro-5-[4-(1-Hydroxycyclobutyl)Phenyl]-1H-Indole-3-Carboxylic Acid is a Highly Selective Substrate for Glucuronidation by UGT1A1, Relative to beta-Estradiol.	PF-6409577	0-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
30194276-0	2018	6-Chloro-5-[4-(1-Hydroxycyclobutyl)Phenyl]-1H-Indole-3-Carboxylic Acid is a Highly Selective Substrate for Glucuronidation by UGT1A1, Relative to beta-Estradiol.	Estradiol	146-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
30194276-4	2018	Studies using a panel of 13 human recombinant UGT (hrUGT) enzymes indicated that PF-06409577 was converted to M1 in a highly selective fashion by UGT1A1, which was further verified in human liver microsomes treated with specific chemical inhibitors, and in different UGT1A1 expressers.	pyrazofurin	81-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
30194276-4	2018	Studies using a panel of 13 human recombinant UGT (hrUGT) enzymes indicated that PF-06409577 was converted to M1 in a highly selective fashion by UGT1A1, which was further verified in human liver microsomes treated with specific chemical inhibitors, and in different UGT1A1 expressers.	pyrazofurin	81-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	267-273
30194276-5	2018	Conversion of PF-06409577 to M1 by UGT1A1 occurred in a relatively selective fashion, compared with beta-estradiol (ES), a conventional probe substrate of UGT1A1.	PF-6409577	14-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
30194276-5	2018	Conversion of PF-06409577 to M1 by UGT1A1 occurred in a relatively selective fashion, compared with beta-estradiol (ES), a conventional probe substrate of UGT1A1.	PF-6409577	14-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
30194276-9	2018	Our results suggest the potential utility of PF-06409477 as a selective probe UGT1A1 substrate for UGT reaction phenotyping and inhibition studies in preclinical discovery/development.	pf-06409477	45-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
30527181-0	2018	Association of nephrotoxicity during platinum-etoposide doublet therapy with UGT1A1 polymorphisms in small cell lung cancer patients.	Platinum	37-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
30527181-0	2018	Association of nephrotoxicity during platinum-etoposide doublet therapy with UGT1A1 polymorphisms in small cell lung cancer patients.	Etoposide	46-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Etoposide	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-53
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Etoposide	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Etoposide	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-53
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Etoposide	231-240	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-53
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Etoposide	231-240	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30527181-10	2018	CONCLUSION: Our results reveal an association between UGT1A1 polymorphisms and toxicity of platinum-etoposide doublet therapy in SCLC patients, suggesting that close monitoring for toxicity, especially nephrotoxicity, is warranted for patients with such variant alleles receiving this treatment.	Platinum	91-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
30527181-10	2018	CONCLUSION: Our results reveal an association between UGT1A1 polymorphisms and toxicity of platinum-etoposide doublet therapy in SCLC patients, suggesting that close monitoring for toxicity, especially nephrotoxicity, is warranted for patients with such variant alleles receiving this treatment.	Etoposide	100-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
30563996-1	2018	Background/objectives: Individuals with Gilbert"s syndrome (GS) harbor mutations in the UGT1A1 gene and are known to have elevated levels of bilirubin, which enhances the risk for gall stone formation.	Bilirubin	141-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	9-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
29955115-0	2018	UGT1A1 polymorphisms associated with prolactin response in risperidone-treated children and adolescents with autism spectrum disorder.	Risperidone	59-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
29955115-8	2018	In this DMET microarray platform, we found three UGT1A1 variants with suggestive evidences of association with the risperidone-induced prolactin response both measured by hyperprolactinemia and by prolactin level.	Risperidone	115-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
30538568-0	2018	Value of plasma SN-38 levels and DPD activity in irinotecan-based individualized chemotherapy for advanced colorectal cancer with heterozygous type UGT1A1*6 or UGT1A1*28.	Irinotecan	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
30538568-0	2018	Value of plasma SN-38 levels and DPD activity in irinotecan-based individualized chemotherapy for advanced colorectal cancer with heterozygous type UGT1A1*6 or UGT1A1*28.	Irinotecan	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	9-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	9-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	9-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-3	2018	Results: CSN-38 1.5h and CSN-38 49h of the UGT1A1*6 or UGT1A1*28 heterozygous type were close to those of UGT1A1*6 and UGT1A1*28 wild-types; some of those with relatively high CSN-38 1.5h levels obtained better median progression-free survival (mPFS), whereas others with higher CSN-38 49h concentrations showed a relatively high incidence of adverse reactions possibly because of the decreased activity of DPD.	4-nitrocatechol sulfate	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30538568-5	2018	For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type.	Fluorouracil	96-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	260-266
30538568-5	2018	For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type.	Fluorouracil	96-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	272-278
30538568-5	2018	For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type.	Fluorouracil	127-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	260-266
30538568-5	2018	For cases with comparably low DPD activity, advisable primary and subsequent dose adjustment of 5-fluorouracil based on plasma 5-fluorouracil levels may be a practical strategy for reducing the occurrence of adverse reactions for personalized treatment of the UGT1A1*6 or UGT1A1*28 heterozygous type.	Fluorouracil	127-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	272-278
32186076-6	2018	YMJHT inhibited CYP2E1 activity, with a negligible inhibition on the activities of CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP3A4, UGT1A1, UGT1A4 and UGT2B7.	ymjht	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
29932297-0	2018	UGT1A1*6 and UGT1A1*28 polymorphisms are correlated with irinotecan-induced toxicity: A meta-analysis.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
29932297-0	2018	UGT1A1*6 and UGT1A1*28 polymorphisms are correlated with irinotecan-induced toxicity: A meta-analysis.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
29932297-1	2018	BACKGROUND: Previous articles explored the role of UGT1A1 polymorphism on predicting irinotecan-induced toxicity, but the conclusions were still inconsistent and not comprehensive.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
29932297-2	2018	We performed this meta-analysis to investigate the association between UGT1A1 polymorphism and irinotecan-induced toxicity.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
29932297-8	2018	Both UGT1A1*6 and UGT1A1*28 polymorphism are significantly associated with severe irinotecan-induced toxicity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
29932297-8	2018	Both UGT1A1*6 and UGT1A1*28 polymorphism are significantly associated with severe irinotecan-induced toxicity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
29932297-12	2018	Subgroup analysis exhibited that for UGT1A1*6 polymorphism, patients treated with low-dose irinotecan were at a notable risk of toxicity.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
29932297-13	2018	Moreover, the association between UGT1A1*6 polymorphism and irinotecan-induced toxicity was found in patients suffering from respiratory system cancers.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
29932297-14	2018	CONCLUSIONS: Both UGT1A1*6 and UGT1A1*28 polymorphisms can be considered as predictors of irinotecan-induced toxicity, with effect varying by race, cancer type and irinotecan dose.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
29932297-14	2018	CONCLUSIONS: Both UGT1A1*6 and UGT1A1*28 polymorphisms can be considered as predictors of irinotecan-induced toxicity, with effect varying by race, cancer type and irinotecan dose.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30266131-1	2018	Crigler-Najjar syndrome type II is caused by mutations in the UGT1A1 gene resulting in severely reduced hepatic activity of UDP-glucoronyltransferase - an enzyme required to convert bilirubin into a more soluble form that can then be removed from the body.	Bilirubin	182-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
29309376-8	2018	In addition, we analyzed bilirubin uridine diphosphate (UDP)-glucuronosyltransferase 1A1 gene that revealed a heterozygous state ([TA]6/[TA]7).	Bilirubin	25-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-88
29273261-1	2018	PURPOSE: We aimed to identify the maximum tolerated dose (MTD) of weekly irinotecan in combination with capecitabine-based neoadjuvant chemoradiation according to the UGT1A1*28 genotype in patients with locally advanced rectal cancer.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
29273261-11	2018	CONCLUSION: A higher dose of weekly irinotecan in combination with capecitabine-based CRT is feasible under the guidance of the UGT1A1*28 genotype.	Irinotecan	36-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
29273261-11	2018	CONCLUSION: A higher dose of weekly irinotecan in combination with capecitabine-based CRT is feasible under the guidance of the UGT1A1*28 genotype.	Capecitabine	67-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
30036684-4	2018	Herein, we designed and optimized a validated cocktail method for the simultaneous evaluation of drug-mediated inhibition of the main five UGT isoforms using respective specific probe substrates (estradiol for UGT1A1, chenodeoxycholic acid for UGT1A3, serotonin for UGT1A6, propofol for UGT1A9/PROG and zidovudine for UGT2B7/AZTG) in human and rat liver microsomes by liquid chromatography-tandem mass spectrometry (LCMS/MS).	Estradiol	196-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	210-216
29951694-1	2018	PURPOSE: Belinostat is a second-generation histone deacetylase inhibitor (HDI) predominantly metabolized by UGT1A1-mediated glucuronidation.	belinostat	9-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
30139029-0	2018	[Relationship between UGT1A1 gene polymorphisms and irinotecan-induced severe adverse events].	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
30139029-1	2018	Objective: To investigate the relationship between UGT1A1*6, UGT1A1*28, UGT1A1*60 and UGT1A1*93 polymorphisms and irinotecan-induced severe adverse reactions(grade 3-4 delayed diarrhea and neutropenia) in Chinese cancer patients.	Irinotecan	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
30139029-16	2018	Conclusion: The cancer patients who carried UGT1A1*6, UGT1A1*28 and UGT1A1*60 gene polymorphisms have high risk of severe adverse events caused by irinotecan-based chemotherapy.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
30139029-16	2018	Conclusion: The cancer patients who carried UGT1A1*6, UGT1A1*28 and UGT1A1*60 gene polymorphisms have high risk of severe adverse events caused by irinotecan-based chemotherapy.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
30139029-16	2018	Conclusion: The cancer patients who carried UGT1A1*6, UGT1A1*28 and UGT1A1*60 gene polymorphisms have high risk of severe adverse events caused by irinotecan-based chemotherapy.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
29735754-5	2018	Conversely, PT-GP and PT-Ac caused direct inhibition of almost all P450 and UGT enzymes, with CYP1A2 (IC50 values of 0.8-4.2 muM), CYP2C8 (IC50 values of 1.1-12 muM), and UGT1A1 (IC50 values of 4.5-5.4 muM) inhibited to the greatest extent.	pt-gp	12-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
29735754-5	2018	Conversely, PT-GP and PT-Ac caused direct inhibition of almost all P450 and UGT enzymes, with CYP1A2 (IC50 values of 0.8-4.2 muM), CYP2C8 (IC50 values of 1.1-12 muM), and UGT1A1 (IC50 values of 4.5-5.4 muM) inhibited to the greatest extent.	6-(3-propylthio-1,2,5-thiadiazol-4-yl)-1-azabicyclo(3.2.1)octane	22-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
29909091-2	2018	We assessed potential clinical variables that may predict toxicity and more specifically the role of UGT1A1 polymorphisms associated with irinotecan toxicity.	Irinotecan	138-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-109
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Fluorouracil	198-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-109
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Fluorouracil	198-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
30334318-0	2018	Efflux excretion of bisdemethoxycurcumin-O-glucuronide in UGT1A1-overexpressing HeLa cells: Identification of breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins 1 (MRP1) as the glucuronide transporters.	bisdemethoxycurcumin-o-glucuronide	20-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
30105461-2	2018	Therefore, it would be beneficial to understand whether there is a relationship between inhibition of uridine-5"-diphosphate glucuronosyltransferase (UGT) 1A1 activity and observed bilirubin elevations in TKI drug-treated patients.	Bilirubin	181-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-158
30105461-3	2018	UGT1A1 is responsible for the glucuronidation of bilirubin which leads to its elimination in the bile.	Bilirubin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
30425912-1	2018	The UGT1A1 enzyme is involved in the metabolism of bilirubin and numerous medications.	Bilirubin	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
30425912-11	2018	Level of bilirubin in pediatric GS patients at diagnosis was UGT1A1 (TA)n promoter genotype-dependent.	Bilirubin	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
30151596-7	2018	Moreover, we demonstrate that UGT1A1, 1A6 and 1A9 proteins catalyze the synthesis of CHZ-O-Glc while CHZ-N-Glc is produced by UGT1A9 specifically.	chz-o-glc	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
29934866-5	2018	The C-terminal domain is identical for all UGT1A family members and required for binding to UDP-glucuronic acid as well as involved in contacts with substrates.	Uridine Diphosphate Glucuronic Acid	92-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-48
30075316-3	2018	Of the 10 tested UGT isoforms, uva-ursi extracts exerted the strongest inhibitory effect on UGT1A1-mediated beta-estradiol 3-glucuronidation with the lowest IC50 value of 8.45 +- 1.56 mug/mL.	Estradiol	108-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
30075316-7	2018	Thus, in vitro UGT1A1 inhibitory potentials of uva-ursi extracts might primarily result from the inhibitory activities of gallotannin and 1,2,3,6-tetragalloylglucose present in the extracts.	Hydrolyzable Tannins	122-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
30075316-7	2018	Thus, in vitro UGT1A1 inhibitory potentials of uva-ursi extracts might primarily result from the inhibitory activities of gallotannin and 1,2,3,6-tetragalloylglucose present in the extracts.	1,2,3,6-tetragalloylglucose	138-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
30117422-1	2018	The adverse reaction to irinotecan is related to the single nucleotide polymorphism (SNP) of UGT1A1*6 genotype.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
30016963-0	2018	Influence of UGT1A1 polymorphisms on the outcome of acute myeloid leukemia patients treated with cytarabine-base regimens.	Cytarabine	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
28891378-15	2018	Ritonavir and cobicistat are unlikely to produce clinically important drug interactions involving drugs metabolized to glucuronide conjugates by UGT1A1, 1A3, 1A6, 1A9, 2B4 and 2B7.	Glucuronides	119-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-43
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	97-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-43
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	193-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-43
30016963-3	2018	METHODS: UGT1A1*6 and *28 polymorphisms resulting in reduced UGT1A1 activity were genotyped in 726 adult acute myeloid leukemia (AML) patients treated with Ara-C based regimens.	Cytarabine	156-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
30016963-5	2018	RESULTS: After one or two courses of Ara-C based induction chemotherapy, the complete remission (CR) rate was significantly higher in patients carrying the UGT1A1*6 (77.0%) or the UGT1A1*28 (76.4%) alleles as compared with corresponding wild-type homozygotes (66.9 and 68.5%, respectively).	Cytarabine	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
30016963-5	2018	RESULTS: After one or two courses of Ara-C based induction chemotherapy, the complete remission (CR) rate was significantly higher in patients carrying the UGT1A1*6 (77.0%) or the UGT1A1*28 (76.4%) alleles as compared with corresponding wild-type homozygotes (66.9 and 68.5%, respectively).	Cytarabine	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
30016963-7	2018	CONCLUSION: Our results suggest that UGT1A1*28 and UGT1A1*6 are associated with improved clinical outcomes in Chinese AML patients treated with Ara-C.	Cytarabine	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
30016963-7	2018	CONCLUSION: Our results suggest that UGT1A1*28 and UGT1A1*6 are associated with improved clinical outcomes in Chinese AML patients treated with Ara-C.	Cytarabine	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
29504153-0	2018	Relevance of CYP3A4*20, UGT1A1*37 and UGT1A1*28 variants in irinotecan-induced severe toxicity.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
30075835-8	2018	Pharmacogenomics guidelines have been published by some international scientific consortia such as the Clinical Pharmacogenomics Implementation Consortium (CPIC) and the Dutch Pharmacogenetics Working Group (DPWG) strongly suggesting a pre-treatment dose adjustment of irinotecan based on UGT1A1*28 genotype and of fluoropyrimidines based on some DPYD genetic variants, to increase treatment safety.	Irinotecan	269-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	289-295
29584932-5	2018	The structure-dependent effects of the hydroxyl flavonoids on induction of UGT1A1 were similar to that observed for induction of CYP1A1 except that luteolin and apigenin induced UGT1A1 levels similar to that observed for TCDD, whereas both compounds were AhR antagonists for CYP1A1.	Flavonoids	48-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
29847509-9	2018	As a positive control, baseline plasma bilirubin concentration was associated with predicted liver UGT1A1 expression level (P=1.9x10(-27)).	Bilirubin	39-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
29420340-11	2018	Patients carrying more than three copies of variant UGT1A1 (*28 and *60) had higher serum levels of belinostat because of slower clearance.	belinostat	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
29504153-0	2018	Relevance of CYP3A4*20, UGT1A1*37 and UGT1A1*28 variants in irinotecan-induced severe toxicity.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
29504153-1	2018	Severe irinotecan-induced toxicity is associated with UGT1A1 polymorphisms.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
29094205-0	2018	Association between alanine aminotransferase elevation and UGT1A1*6 polymorphisms in daclatasvir and asunaprevir combination therapy for chronic hepatitis C. BACKGROUND: Liver damage presented as alanine aminotransferase (ALT) elevation and high ALT-caused treatment discontinuation occurs with high frequency in Japanese patients receiving daclatasvir plus asunaprevir (DCV/ASV) therapy for hepatitis C virus (HCV) infection, and its mechanism is unknown.	daclatasvir	85-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
29637732-2	2018	Delivery of hUGT1A1-modRNA (a modified messenger RNA encoding for UGT1A1) as a lipid nanoparticle is anticipated to restore hepatic expression of UGT1A1, allowing normal glucuronidation and clearance of bilirubin in patients.	Bilirubin	203-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-19
29637732-2	2018	Delivery of hUGT1A1-modRNA (a modified messenger RNA encoding for UGT1A1) as a lipid nanoparticle is anticipated to restore hepatic expression of UGT1A1, allowing normal glucuronidation and clearance of bilirubin in patients.	Bilirubin	203-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
29637732-2	2018	Delivery of hUGT1A1-modRNA (a modified messenger RNA encoding for UGT1A1) as a lipid nanoparticle is anticipated to restore hepatic expression of UGT1A1, allowing normal glucuronidation and clearance of bilirubin in patients.	Bilirubin	203-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
29094205-0	2018	Association between alanine aminotransferase elevation and UGT1A1*6 polymorphisms in daclatasvir and asunaprevir combination therapy for chronic hepatitis C. BACKGROUND: Liver damage presented as alanine aminotransferase (ALT) elevation and high ALT-caused treatment discontinuation occurs with high frequency in Japanese patients receiving daclatasvir plus asunaprevir (DCV/ASV) therapy for hepatitis C virus (HCV) infection, and its mechanism is unknown.	asunaprevir	101-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
29094205-5	2018	CONCLUSIONS: Through the analysis we suggest that the A allele in UGT1A1 rs4148323 (UGT1A1*6), which is highly prevalent in the Japanese population, should be considered a risk for the development of DCV/ASV therapy-induced ALT elevation.	daclatasvir	200-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
29094205-5	2018	CONCLUSIONS: Through the analysis we suggest that the A allele in UGT1A1 rs4148323 (UGT1A1*6), which is highly prevalent in the Japanese population, should be considered a risk for the development of DCV/ASV therapy-induced ALT elevation.	daclatasvir	200-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
29094205-5	2018	CONCLUSIONS: Through the analysis we suggest that the A allele in UGT1A1 rs4148323 (UGT1A1*6), which is highly prevalent in the Japanese population, should be considered a risk for the development of DCV/ASV therapy-induced ALT elevation.	asunaprevir	204-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
29094205-5	2018	CONCLUSIONS: Through the analysis we suggest that the A allele in UGT1A1 rs4148323 (UGT1A1*6), which is highly prevalent in the Japanese population, should be considered a risk for the development of DCV/ASV therapy-induced ALT elevation.	asunaprevir	204-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	daclatasvir	103-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	asunaprevir	107-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	daclatasvir	122-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	asunaprevir	126-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	8-cyclohexyl-N-((dimethylamino)sulfonyl)-1,1a,2,12b-tetrahydro-11-methoxy-1a-((3-methyl-3,8-diazabicyclo(3.2.1)oct-8-yl)carbonyl)cycloprop(d)indolo(2,1-a)(2)benzazepine-5-carboxamide	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29743555-1	2018	The aim of this study was to evaluate the effect of UGT1A1 polymorphisms on Raltegravir (RAL) and its metabolite RAL-glucuronide trough plasma concentrations ([RAL]plasma and [RAL-glu]plasma) and on the metabolic ratio (MR): [RAL-glu]plasma/[RAL]plasma.	Glutamic Acid	117-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
29587224-6	2018	Besides, icaritin glucuronidation is mediated by multiple enzymes, with UGT1A1 the principal metabolizing enzyme (total CLint,UGT1A1 = 6.38 mL/mg/min).	icaritin	9-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
29587224-6	2018	Besides, icaritin glucuronidation is mediated by multiple enzymes, with UGT1A1 the principal metabolizing enzyme (total CLint,UGT1A1 = 6.38 mL/mg/min).	icaritin	9-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
29743555-0	2018	Impact of UGT1A1 polymorphisms on Raltegravir and its glucuronide plasma concentrations in a cohort of HIV-1 infected patients.	Raltegravir Potassium	34-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
28548030-5	2018	The results showed that 100 muM of everolimus exerted more than 80% inhibition toward UGT1A1, UGT-1A3 and UGT-2B7.	Everolimus	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
29743555-0	2018	Impact of UGT1A1 polymorphisms on Raltegravir and its glucuronide plasma concentrations in a cohort of HIV-1 infected patients.	Glucuronides	54-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
29743555-1	2018	The aim of this study was to evaluate the effect of UGT1A1 polymorphisms on Raltegravir (RAL) and its metabolite RAL-glucuronide trough plasma concentrations ([RAL]plasma and [RAL-glu]plasma) and on the metabolic ratio (MR): [RAL-glu]plasma/[RAL]plasma.	Raltegravir Potassium	76-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
29743555-1	2018	The aim of this study was to evaluate the effect of UGT1A1 polymorphisms on Raltegravir (RAL) and its metabolite RAL-glucuronide trough plasma concentrations ([RAL]plasma and [RAL-glu]plasma) and on the metabolic ratio (MR): [RAL-glu]plasma/[RAL]plasma.	ral-glucuronide	113-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
28548030-8	2018	The inhibition kinetic parameters (Ki) were calculated to be 2.3, 0.07 and 4.4 muM for the inhibition of everolimus toward UGT1A1, UGT-1A3 and UGT-2B7, respectively.	Everolimus	105-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
28520360-0	2012	Irinotecan Therapy and UGT1A1 Genotype Irinotecan is a topoisomerase inhibitor that is widely used in the treatment of cancer.	Irinotecan	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
29702735-2	2018	We investigated whether the variant genotypes of metabolic enzymes UGT1A1, CYP3A5 and transporter ABCB1 influence pharmacokinetic phenotype of substrate mizolastine in Chinese volunteers.	mizolastine	153-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
28520360-3	2012	Irinotecan is metabolized and inactivated by an UDP-glucuronosyltransferase enzyme encoded by the gene UGT1A1.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
28520360-5	2012	Variants of this gene, such as UGT1A1*28, are associated with reduced enzyme activity and an increased risk of irinotecan toxicity.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
28520360-6	2012	Approximately 10% of North Americans are homozygous for the UGT1A1*28 allele and are more likely to develop neutropenia following irinotecan therapy (3).	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
28520360-7	2012	The FDA-approved drug label for irinotecan states that "when administered as a single-agent, a reduction in the starting dose by at least one level of irinotecan hydrochloride injection should be considered for patients known to be homozygous for the UGT1A1*28 allele.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
28520360-7	2012	The FDA-approved drug label for irinotecan states that "when administered as a single-agent, a reduction in the starting dose by at least one level of irinotecan hydrochloride injection should be considered for patients known to be homozygous for the UGT1A1*28 allele.	Irinotecan	151-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
28520360-9	2012	A guideline from the Dutch Pharmacogenetics Working Group (KNMP) mentions "although results are not consistent, there is sufficient evidence that a reduction in the initial dose by 30% is required for regimens containing &gt;250 mg/m(2) of irinotecan prescribed to homozygous carriers of the UGT1A1*28 allele.	Irinotecan	240-250	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	292-298
29328989-4	2018	100 muM phthalate monoesters exhibited negligible inhibition towards the activity of UGT1A1, UGT1A3, UGT1A6, UGT1A8, UGT1A10, UGT2B4, UGT2B7, UGT2B15 and UGT2B17.	phthalic acid	8-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
29161598-10	2018	However, selenium supplementation led to elevations of selenium, Dio1 and TTR, and reductions of Ugt1a1, Sult1e1, CYP2b1, and TRHr.	Selenium	9-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
29311138-0	2018	Bacterial Outer Membrane Vesicles from Dextran Sulfate Sodium-Induced Colitis Differentially Regulate Intestinal UDP-Glucuronosyltransferase 1A1 Partially Through Toll-Like Receptor 4/Mitogen-Activated Protein Kinase/Phosphatidylinositol 3-Kinase Pathway.	Dextran Sulfate	39-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-144
29220881-6	2018	RESULTS: As expected, UGT1A1 genotypes were associated with baseline bilirubin levels (*1/*1 genotype: 9.1+-4.6 micromol/L; *1/*28 genotype: 10.8+-5.3; *28/*28: 16.9+-9.2; p&lt;0.001).	Bilirubin	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
29220881-8	2018	In a multivariate regression analysis adjusting for age, sex, smoking, type 2 diabetes, dyslipidemia, alanine aminotransferase (ALT) levels and bilirubin levels, the UGT1A1*28 variant predicted lower overall mortality (hazard ratio [HR], 0.86; 95% confidence interval [CI], 0.78-0.95; p=0.003).	Bilirubin	144-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
29220881-11	2018	The protective effect of the UGT1A1*28 variant likely includes mechanism other than bilirubin metabolism.	Bilirubin	84-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
29524031-0	2018	Contribution of UGT1A1 genetic polymorphisms related to axitinib pharmacokinetics to safety and efficacy in patients with renal cell carcinoma.	Axitinib	56-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
29524031-5	2018	Genetic polymorphisms related to axitinib pharmacokinetics, including SLCO1B1, SLCO1B3, SLCO2B1, ABCB1, ABCG2, CYP2C19, CYP3A5, and UGT1A1, were analyzed.	Axitinib	33-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
29524031-9	2018	Genetic polymorphisms in UGT1A1 were significantly associated with the plasma axitinib level.	Axitinib	78-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
29318243-0	2018	Chemical inhibition and stable knock-down of efflux transporters leads to reduced glucuronidation of wushanicaritin in UGT1A1-overexpressing HeLa cells: the role of breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins (MRPs) in the excretion of glucuronides.	wushanicaritin	101-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
29223776-0	2018	Impact of edaphic factors and nutrient management on the hepatoprotective efficiency of Carlinoside purified from pigeon pea leaves: An evaluation of UGT1A1 activity in hepatitis induced organelles.	carlinoside	88-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
28285550-13	2018	Stronger hydrogen bonds and hydrophobic interaction between T4 and activity cavity of UGT1A1 than T3 contributed to stronger inhibition of T4 towards UGT1A1.	Hydrogen	9-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
28285550-13	2018	Stronger hydrogen bonds and hydrophobic interaction between T4 and activity cavity of UGT1A1 than T3 contributed to stronger inhibition of T4 towards UGT1A1.	Hydrogen	9-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
29425147-5	2018	In human liver microsomes (HLMs), sauchinone inhibited activities of UGT1A1, 1A3, 1A6, and 2B7 with IC50 values of 8.83, 43.9, 0.758, and 0.279 muM, respectively.	sauchinone	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
29223776-7	2018	This significantly up-regulated the carlinoside induced expression of the bilirubin-solubilizing UGT1A1enzyme in HepG2 cell and rat liver.	carlinoside	36-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
29223776-7	2018	This significantly up-regulated the carlinoside induced expression of the bilirubin-solubilizing UGT1A1enzyme in HepG2 cell and rat liver.	Bilirubin	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
29114966-5	2018	The UGT1A1 (TA)6 /(TA)8 heterozygote showed statistically significant associations with HbA2 levels (P = .019), HbF percentage (P &lt; .001), haemoglobin levels (P = .008), PCV values (P = .007) and RBC counts (P = .041).	penciclovir	173-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-57
29239247-7	2018	The rates of 7TA carriers of UGT1A1 rs8175347 in all three groups were significantly higher than the other genotypes.	SCHEMBL3705488	13-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
29124328-1	2018	PURPOSE: We aimed to retrospectively evaluate the efficacy and toxicity of an irinotecan hydrochloride (CPT) and nedaplatin (N) combination therapy for recurrent and refractory endometrial carcinoma, administered based on UGT1A1 genotype.	Irinotecan	78-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
29124328-1	2018	PURPOSE: We aimed to retrospectively evaluate the efficacy and toxicity of an irinotecan hydrochloride (CPT) and nedaplatin (N) combination therapy for recurrent and refractory endometrial carcinoma, administered based on UGT1A1 genotype.	cpt	104-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
29124328-9	2018	Patients with a wild-type UGT1A1 status received higher doses of CPT-11 (p = 0.048) and had similar RR and CBR compared to those with a UGT1A1*6 and *28 status.	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
29589315-7	2018	It has been established that UGT1A1*28 polymorphism is associated with irinotecan toxicity, but this test is rarely performed as the management strategy has not been identified.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
29117017-9	2018	CONCLUSION: Among patients who initiated atazanavir/ritonavir-containing regimens, UGT1A1 slow metabolizer genotype rs887829 T/T was associated with increased bilirubin-related discontinuation of atazanavir in White but not in Black patients, this despite T/T genotype being more frequent in Black patients.	Atazanavir Sulfate	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
29117017-9	2018	CONCLUSION: Among patients who initiated atazanavir/ritonavir-containing regimens, UGT1A1 slow metabolizer genotype rs887829 T/T was associated with increased bilirubin-related discontinuation of atazanavir in White but not in Black patients, this despite T/T genotype being more frequent in Black patients.	Ritonavir	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
29117017-9	2018	CONCLUSION: Among patients who initiated atazanavir/ritonavir-containing regimens, UGT1A1 slow metabolizer genotype rs887829 T/T was associated with increased bilirubin-related discontinuation of atazanavir in White but not in Black patients, this despite T/T genotype being more frequent in Black patients.	Bilirubin	159-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
29117017-9	2018	CONCLUSION: Among patients who initiated atazanavir/ritonavir-containing regimens, UGT1A1 slow metabolizer genotype rs887829 T/T was associated with increased bilirubin-related discontinuation of atazanavir in White but not in Black patients, this despite T/T genotype being more frequent in Black patients.	Atazanavir Sulfate	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
29052349-0	2018	Relationship between UGT1A1*27 and UGT1A1*7 polymorphisms and irinotecan-related toxicities in patients with lung cancer.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
29052349-0	2018	Relationship between UGT1A1*27 and UGT1A1*7 polymorphisms and irinotecan-related toxicities in patients with lung cancer.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
29052349-1	2018	BACKGROUND: The objective of this study was to evaluate the effects of gene polymorphisms, including UGT1A1*7, *27, and *29, on the safety of irinotecan therapy.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
29052349-8	2018	SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
29052349-8	2018	SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
29052349-8	2018	SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
29052349-10	2018	CONCLUSION: UGT1A1*27 can occur separately from UGT1A1*28 and is related to leukopenia during irinotecan treatment.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
29052349-10	2018	CONCLUSION: UGT1A1*27 can occur separately from UGT1A1*28 and is related to leukopenia during irinotecan treatment.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29052349-11	2018	UGT1A1*7 is less relevant to irinotecan-induced toxicities, and UGT1A1*29 seems to have little clinical impact.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28689454-12	2018	Considering the above findings and the current knowledge on UGTs expression in HIM, it is likely that UGT1A10 is mainly responsible for xanthotoxol glucuronidation in the human small intestine, with some contribution from UGT1A1.	xanthotoxol	136-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
29891024-10	2018	Previous reports, studies of recombinant UGT isoforms indicated that SN-38 glucuronidation was mainly catalyzed by UGT1A1.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
30673201-4	2018	On the other hand, carriers of various genotypes of UGT1A1 differ significantly in metabolism characteristics of a number of common medications (irinotecan, belinostat, etc.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
30673201-4	2018	On the other hand, carriers of various genotypes of UGT1A1 differ significantly in metabolism characteristics of a number of common medications (irinotecan, belinostat, etc.	belinostat	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
29487697-5	2018	Present results support the preemptive screening of mentioned DPYD and UGT1A1 variants to identify patients at risk of clinically relevant 5-fluoruracil- and irinotecan-related AEs, in order to improve treatments" safety through a "genotype-guided" approach.	Fluorouracil	139-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
29487697-5	2018	Present results support the preemptive screening of mentioned DPYD and UGT1A1 variants to identify patients at risk of clinically relevant 5-fluoruracil- and irinotecan-related AEs, in order to improve treatments" safety through a "genotype-guided" approach.	Irinotecan	158-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
29025858-1	2017	Human UDP-glucuronosyltransferase 1A1 (UGT1A1) is a unique enzyme involved in bilirubin conjugation.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-37
29125289-0	2017	A Practical and High-Affinity Fluorescent Probe for Uridine Diphosphate Glucuronosyltransferase 1A1: A Good Surrogate for Bilirubin.	Bilirubin	122-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-99
29125289-2	2017	Several substrates derived from N-butyl-4-phenyl-1,8-naphthalimide were designed and synthesized on the basis of the substrate preference of UGT1A1 and the principle of photoinduced electron transfer (PET).	n-butyl-4-phenyl-1,8-naphthalimide	32-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
29125289-4	2017	Both inhibition kinetic analyses and molecular docking simulations demonstrated that 2 could bind on UGT1A1 at the same ligand-binding site as bilirubin.	Bilirubin	143-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
29125289-6	2017	In conclusion, a practical and high-affinity fluorescent probe for UGT1A1 was designed and well-characterized, which could serve as a good surrogate for bilirubin to investigate UGT1A1-ligand interactions.	Bilirubin	153-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
29025858-1	2017	Human UDP-glucuronosyltransferase 1A1 (UGT1A1) is a unique enzyme involved in bilirubin conjugation.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
29159025-4	2017	The results demonstrated that both icotinib and erlotinib are UGT1A1 inhibitors, but the inhibitory effect of icotinib on UGT1A1 is weaker than that of erlotinib.	icotinib	35-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
29133521-10	2017	A genetic variant at the UGT1A1*28 locus consistently shown to be strongly associated with circulating bilirubin levels-rs6742078-was not significantly associated with blood pressure or hypertension (P&gt;0.05 for all), arguing against a strong causal association of circulating bilirubin with blood pressure.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
28536775-7	2017	Meantime, oroxylin A was rapidly metabolized by UGTs, UGT1A1, -1A3, -1A6, -1A7, -1A8, -1A9, and -1A10 which were involved in the glucuronidation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	10-20	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
28990653-0	2017	Mechanism of in-vitro inhibition of UGT1A1 by paritaprevir.	paritaprevir	46-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
28990653-2	2017	Paritaprevir is reported to inhibit human UGT 1A1, but the mechanism of inhibition and its possible clinical consequences are not established.	paritaprevir	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-49
28990653-3	2017	Our objective was to evaluate the in-vitro metabolic interaction between paritaprevir and the oral contraceptive steroid ethinyl estradiol (EE), a UGT 1A1 substrate.	paritaprevir	73-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-154
28990653-3	2017	Our objective was to evaluate the in-vitro metabolic interaction between paritaprevir and the oral contraceptive steroid ethinyl estradiol (EE), a UGT 1A1 substrate.	Steroids	113-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-154
28990653-3	2017	Our objective was to evaluate the in-vitro metabolic interaction between paritaprevir and the oral contraceptive steroid ethinyl estradiol (EE), a UGT 1A1 substrate.	Ethinyl Estradiol	121-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-154
28990653-9	2017	CONCLUSIONS: Paritaprevir is an in-vitro inhibitor of UGT 1A1.	paritaprevir	13-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-61
29159025-0	2017	Comparison of the inhibition potentials of icotinib and erlotinib against human UDP-glucuronosyltransferase 1A1.	icotinib	43-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-111
29159025-0	2017	Comparison of the inhibition potentials of icotinib and erlotinib against human UDP-glucuronosyltransferase 1A1.	Erlotinib Hydrochloride	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-111
29159025-4	2017	The results demonstrated that both icotinib and erlotinib are UGT1A1 inhibitors, but the inhibitory effect of icotinib on UGT1A1 is weaker than that of erlotinib.	Erlotinib Hydrochloride	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
29159025-3	2017	This study aimed to investigate and compare the inhibitory effects of icotinib and erlotinib against UGT1A1, as well as to evaluate their potential DDI risks via UGT1A1 inhibition.	icotinib	70-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
29159025-3	2017	This study aimed to investigate and compare the inhibitory effects of icotinib and erlotinib against UGT1A1, as well as to evaluate their potential DDI risks via UGT1A1 inhibition.	Erlotinib Hydrochloride	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
29159025-4	2017	The results demonstrated that both icotinib and erlotinib are UGT1A1 inhibitors, but the inhibitory effect of icotinib on UGT1A1 is weaker than that of erlotinib.	icotinib	110-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
29159025-5	2017	The IC50 values of icotinib and erlotinib against UGT1A1-mediated NCHN-O-glucuronidation in human liver microsomes (HLMs) were 5.15 and 0.68 mumol/L, respectively.	icotinib	19-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
29159025-5	2017	The IC50 values of icotinib and erlotinib against UGT1A1-mediated NCHN-O-glucuronidation in human liver microsomes (HLMs) were 5.15 and 0.68 mumol/L, respectively.	Erlotinib Hydrochloride	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
29159025-5	2017	The IC50 values of icotinib and erlotinib against UGT1A1-mediated NCHN-O-glucuronidation in human liver microsomes (HLMs) were 5.15 and 0.68 mumol/L, respectively.	nchn-o	66-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
29159025-6	2017	Inhibition kinetic analyses demonstrated that both icotinib and erlotinib were non-competitive inhibitors against UGT1A1-mediated glucuronidation of NCHN in HLMs, with the Ki values of 8.55 and 1.23 mumol/L, respectively.	icotinib	51-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
29159025-6	2017	Inhibition kinetic analyses demonstrated that both icotinib and erlotinib were non-competitive inhibitors against UGT1A1-mediated glucuronidation of NCHN in HLMs, with the Ki values of 8.55 and 1.23 mumol/L, respectively.	Erlotinib Hydrochloride	64-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
29159025-6	2017	Inhibition kinetic analyses demonstrated that both icotinib and erlotinib were non-competitive inhibitors against UGT1A1-mediated glucuronidation of NCHN in HLMs, with the Ki values of 8.55 and 1.23 mumol/L, respectively.	nchn	149-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
29159025-8	2017	These findings are helpful for the medicinal chemists to design and develop next generation tyrosine kinase inhibitors with improved safety, as well as to guide reasonable applications of icotinib and erlotinib in clinic, especially for avoiding their potential DDI risks via UGT1A1 inhibition.	icotinib	188-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	276-282
29159025-8	2017	These findings are helpful for the medicinal chemists to design and develop next generation tyrosine kinase inhibitors with improved safety, as well as to guide reasonable applications of icotinib and erlotinib in clinic, especially for avoiding their potential DDI risks via UGT1A1 inhibition.	Erlotinib Hydrochloride	201-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	276-282
28934153-9	2017	Selaginellin and selaginellin M also showed medium inhibitory potential against CYP2C9, CYP2J2, UGT1A1, and UGT1A3 (1 muM &lt; IC50 &lt; 5 muM).	selaginellin S	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
29113203-1	2017	Uridine diphosphate glucuronosyltransferase 1A (UGT1A1), which affects irinotecan metabolism, has been associated with severe adverse reactions in patients with cancer treated with irinotecan.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-1	2017	Uridine diphosphate glucuronosyltransferase 1A (UGT1A1), which affects irinotecan metabolism, has been associated with severe adverse reactions in patients with cancer treated with irinotecan.	Irinotecan	181-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	222-232	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
29072417-1	2017	Irinotecan life threatening toxicity is partly related to cytotoxic drugmetabolite which is primarily inactivated by the UGT1A1 enzyme.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
29072417-1	2017	Irinotecan life threatening toxicity is partly related to cytotoxic drugmetabolite which is primarily inactivated by the UGT1A1 enzyme.	drugmetabolite	68-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
29072417-2	2017	The primary aim of the present research was tofind the correlation between UGT1A1-genotype and clinical toxicity of irinotecan.	Irinotecan	116-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
29072417-13	2017	Conclusions: UGT1A1 28*/28* is strongly associatedwith drug"s life-threatening toxicity even in a moderate dose of Irinotecan.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
28934153-9	2017	Selaginellin and selaginellin M also showed medium inhibitory potential against CYP2C9, CYP2J2, UGT1A1, and UGT1A3 (1 muM &lt; IC50 &lt; 5 muM).	selaginellin M	17-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
28932176-2	2017	The present research was aimed to study the effect of 2 important single nucleotide polymorphisms (SNPs; rs8330 and rs10929303) of UGT1A1 gene on glucuronidation status of acetaminophen in healthy volunteers (n = 109).	Acetaminophen	172-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
28493308-9	2017	CONCLUSIONS: UGT1A1 genotype-directed dosing (gCAPIRINOX) appears to be feasible with favorable rates of hematologic toxicity compared with prior 3-drug studies in unselected patients.	gcapirinox	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
28915895-0	2017	Impact of UGT1A1 gene polymorphisms on plasma dolutegravir trough concentrations and neuropsychiatric adverse events in Japanese individuals infected with HIV-1.	dolutegravir	46-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
28915895-1	2017	BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A).	dolutegravir	12-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-109
28915895-1	2017	BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A).	dolutegravir	12-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
28915895-1	2017	BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A).	dolutegravir	26-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-109
28915895-1	2017	BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A).	dolutegravir	26-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
28915895-10	2017	Multivariate analysis revealed that carrying one or two UGT1A1*6 gene polymorphisms, one UGT1A1*28 polymorphism, and age of &lt; 40 years were independent factors associated with high DTG trough concentrations.	dolutegravir	184-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
28915895-10	2017	Multivariate analysis revealed that carrying one or two UGT1A1*6 gene polymorphisms, one UGT1A1*28 polymorphism, and age of &lt; 40 years were independent factors associated with high DTG trough concentrations.	dolutegravir	184-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
28915895-13	2017	CONCLUSION: In addition to younger age, carrying UGT1A1*6 and/or UGT1A1*28 was demonstrated to be a factor associated with high DTG trough concentrations.	dolutegravir	128-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
28915895-13	2017	CONCLUSION: In addition to younger age, carrying UGT1A1*6 and/or UGT1A1*28 was demonstrated to be a factor associated with high DTG trough concentrations.	dolutegravir	128-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
28932176-4	2017	The in vivo activity of UGT1A1 was investigated by high-performance liquid chromatography-based analysis of glucuronidation status (ie, acetaminophen and acetaminophen glucuronide) in human volunteers after oral intake of a single dose (1000 mg) of acetaminophen.	Acetaminophen	136-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28932176-4	2017	The in vivo activity of UGT1A1 was investigated by high-performance liquid chromatography-based analysis of glucuronidation status (ie, acetaminophen and acetaminophen glucuronide) in human volunteers after oral intake of a single dose (1000 mg) of acetaminophen.	acetaminophen glucuronide	154-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28932176-4	2017	The in vivo activity of UGT1A1 was investigated by high-performance liquid chromatography-based analysis of glucuronidation status (ie, acetaminophen and acetaminophen glucuronide) in human volunteers after oral intake of a single dose (1000 mg) of acetaminophen.	Acetaminophen	154-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28474802-0	2017	Rapid and sensitive detection of UGT1A1 polymorphisms associated with irinotecan toxicity by a novel DNA microarray.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
28552915-13	2017	This study demonstrates that UGT2B7 common SNPs and their dimers with UGT1A1 and UGT1A9 and their allelic variants can regioselectively affect the generation of two metabolites of morphine via altering the CLint ratios of M3G to M6G.	Morphine	180-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
28567595-0	2017	Do Alpha Thalassemia, Fetal Hemoglobin, and the UGT1A1 Polymorphism have an Influence on Serum Bilirubin Levels and Cholelithiasis in Patients with Sickle Cell Disease?	Bilirubin	95-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
28567595-2	2017	OBJECTIVES: The objective of this study was to determine the combined influence of alpha thalassemia, fetal hemoglobin, and the UGT1A1 polymorphism on serum bilirubin levels and cholelithiasis in patients with sickle cell disease.	Bilirubin	157-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
28567595-6	2017	Bilirubin levels were influenced by the UGT1A1 polymorphism but not by alpha thalassemia and fetal hemoglobin.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
28567595-8	2017	CONCLUSION: These preliminary findings suggest that the UGT1A1 gene can influence serum bilirubin levels in sickle cell anemia and serve as a tool to differentiate an acute hemolytic condition from a pre-existing condition of hyperbilirubinemia.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
28603997-0	2017	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by Polyphenolic Acids Impact Safety of Popular Salvianolic Acid A/B-Containing Drugs and Herbal Products.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28603997-0	2017	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by Polyphenolic Acids Impact Safety of Popular Salvianolic Acid A/B-Containing Drugs and Herbal Products.	polyphenolic acids	65-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28603997-0	2017	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by Polyphenolic Acids Impact Safety of Popular Salvianolic Acid A/B-Containing Drugs and Herbal Products.	salvianolic acid A	109-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28603997-0	2017	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by Polyphenolic Acids Impact Safety of Popular Salvianolic Acid A/B-Containing Drugs and Herbal Products.	Boron	36-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28603997-3	2017	The purpose of this article is to determine the mechanism by which certain polyphenolic acids inhibit UGT1A1-mediated bilirubin glucuronidation, leading to jaundice or hyperbilirubinemia.	polyphenolic acids	75-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
28603997-3	2017	The purpose of this article is to determine the mechanism by which certain polyphenolic acids inhibit UGT1A1-mediated bilirubin glucuronidation, leading to jaundice or hyperbilirubinemia.	Bilirubin	118-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
28603997-6	2017	SAA, SAB, DSI, and CDI, but not DSS, PA, and RA, significantly inhibited human UGT1A1-mediated bilirubin glucuronidation via a mixed-type inhibitory mechanism.	salvianolic acid B	5-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
28603997-6	2017	SAA, SAB, DSI, and CDI, but not DSS, PA, and RA, significantly inhibited human UGT1A1-mediated bilirubin glucuronidation via a mixed-type inhibitory mechanism.	N-hydroxysuccinimide suberic acid ester	10-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
28603997-6	2017	SAA, SAB, DSI, and CDI, but not DSS, PA, and RA, significantly inhibited human UGT1A1-mediated bilirubin glucuronidation via a mixed-type inhibitory mechanism.	Bilirubin	95-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
28654297-7	2017	Recombinant human uridine-5"-diphospho -glucuronosyltransferase (UGT) isoforms and chemical inhibition studies demonstrated that UGT1As (mainly UGT1A1, UGT1A9, UGT1A10) and UGT2B7 were likely the main contributors to eriodictyol glucuronidation.	eriodictyol	217-228	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-133
28397089-9	2017	CONCLUSION: The VCS confirmed the importance of genetic polymorphisms of UGT1A1 *28 and SLCO1B1 c.521T&gt;C in the irinotecan induced side effects.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28585035-0	2017	UGT1A1*6 polymorphisms are correlated with irinotecan-induced neutropenia: a systematic review and meta-analysis.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28474802-4	2017	It is established that the polymorphisms of UGT1A1*28 and UGT1A1*6 are significantly associated with severe toxicity induced by the anti-cancer drug irinotecan.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
28474802-4	2017	It is established that the polymorphisms of UGT1A1*28 and UGT1A1*6 are significantly associated with severe toxicity induced by the anti-cancer drug irinotecan.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
28157715-0	2017	Combined use of irinotecan with histone deacetylase inhibitor belinostat could cause severe toxicity by inhibiting SN-38 glucuronidation via UGT1A1.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
28074472-0	2017	Cost Evaluation of Irinotecan-Related Toxicities Associated With the UGT1A1*28 Patient Genotype.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
28074472-1	2017	The adoption of a preemptive UGT1A1*28 genotyping to increase irinotecan safety in clinical practice is still limited.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
28892962-2	2017	It is caused by mutations in the UGT1A1 gene which codes for the enzyme uridine diphosphate glucoronosyl transferase- 1, required for the conjugation and further excretion of bilirubin from the body.	Bilirubin	175-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
28637434-11	2017	In the first-line irinotecan-based treatment, UGT1A1*28 and DPYD*5 contributed to higher response rates (P = 0.043 and P = 0.019, respectively), while DPYD*5 was found to associate with better progression-free survival (P = 0.015).	Irinotecan	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
28637434-13	2017	CONCLUSION: Results still showed UGT1A1*6 and UGT1A1*28 to be partially associated with irinotecan-induced toxicity and clinical response.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
28637434-13	2017	CONCLUSION: Results still showed UGT1A1*6 and UGT1A1*28 to be partially associated with irinotecan-induced toxicity and clinical response.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
28804517-8	2017	It is imperative to check UGT1A1 gene status in all patients being considered for treatment with nanoliposomal irinotecan.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28157715-0	2017	Combined use of irinotecan with histone deacetylase inhibitor belinostat could cause severe toxicity by inhibiting SN-38 glucuronidation via UGT1A1.	belinostat	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
28157715-4	2017	The data showed that belinostat at 100 and 200 micromol/L inhibited SN-38 glucuronidation via UGT1A1 in a dose-dependent manner, causing significant decrease in Vmax and CLint (p &lt; 0.05) from 12.60 to 1.95 pmol/min/mg and 21.59 to 4.20 muL/min/mg protein respectively.	belinostat	21-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
28157715-4	2017	The data showed that belinostat at 100 and 200 micromol/L inhibited SN-38 glucuronidation via UGT1A1 in a dose-dependent manner, causing significant decrease in Vmax and CLint (p &lt; 0.05) from 12.60 to 1.95 pmol/min/mg and 21.59 to 4.20 muL/min/mg protein respectively.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
28790841-0	2017	Relationship between UGT1A1*6/*28 gene polymorphisms and the efficacy and toxicity of irinotecan-based chemotherapy.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
28790862-6	2017	Pharmacokinetics for additional HIV drugs, such as the integrase inhibitors Raltegravir and Elvitegravir, has been also shown to be influenced by UGT1A1 polymorphisms.	Raltegravir Potassium	76-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
28790862-6	2017	Pharmacokinetics for additional HIV drugs, such as the integrase inhibitors Raltegravir and Elvitegravir, has been also shown to be influenced by UGT1A1 polymorphisms.	elvitegravir	92-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
28790841-1	2017	PURPOSE: A retrospective study was performed to analyze the relationship between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *6/*28 gene polymorphisms and adverse reactions associated with irinotecan (CPT-11)-based chemotherapy.	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-128
28790841-1	2017	PURPOSE: A retrospective study was performed to analyze the relationship between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *6/*28 gene polymorphisms and adverse reactions associated with irinotecan (CPT-11)-based chemotherapy.	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
28790841-1	2017	PURPOSE: A retrospective study was performed to analyze the relationship between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *6/*28 gene polymorphisms and adverse reactions associated with irinotecan (CPT-11)-based chemotherapy.	Irinotecan	214-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-128
28790841-2	2017	The correlation between UGT1A1 polymorphisms and the clinical efficacy of CPT-11 was also analyzed, along with the influence of age and tumor type.	Irinotecan	74-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28790841-5	2017	RESULTS: Colorectal cancer patients with the UGT1A1*6 mutant genotype had a significantly higher risk of severe delayed diarrhea than that of wild-type individuals when administered a CPT-11 dose &gt;=130 mg/m2 (P=0.042); the same phenomenon was observed when the UGT1A1*6 and UGT1A1*28 mutant genotypes were considered together (P=0.028).	Irinotecan	184-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
28790841-5	2017	RESULTS: Colorectal cancer patients with the UGT1A1*6 mutant genotype had a significantly higher risk of severe delayed diarrhea than that of wild-type individuals when administered a CPT-11 dose &gt;=130 mg/m2 (P=0.042); the same phenomenon was observed when the UGT1A1*6 and UGT1A1*28 mutant genotypes were considered together (P=0.028).	Irinotecan	184-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
28790841-5	2017	RESULTS: Colorectal cancer patients with the UGT1A1*6 mutant genotype had a significantly higher risk of severe delayed diarrhea than that of wild-type individuals when administered a CPT-11 dose &gt;=130 mg/m2 (P=0.042); the same phenomenon was observed when the UGT1A1*6 and UGT1A1*28 mutant genotypes were considered together (P=0.028).	Irinotecan	184-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
28790841-6	2017	However, in lung cancer patients administered a low dose of CPT-11, UGT1A1*6/*28 variants were not significantly associated with severe neutropenia or delayed diarrhea.	Irinotecan	60-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28213806-4	2017	The presence of two UGT1A1 variants (consistent with Gilbert or Crigler-Najjar syndrome) occurred less frequently in neonates (aged &lt;=28 days) than older children (aged 1-18 years) (31.3% in neonates vs. 85.1%, p &lt; 0.0001), and among neonates there was no significant difference in mean total bilirubin between those with two UGT1A1 variants and those without (p = 0.47).	Bilirubin	299-308	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28283499-8	2017	In addition to NGMN, we have also elucidated the biotransformation of norgestrel (NG), a downstream norgestimate and NGMN metabolite, and found that CYP3A4 and UGT1A1 have a major contribution to the elimination of NG with a combined fm value of 1.	Norgestrel	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
28283499-8	2017	In addition to NGMN, we have also elucidated the biotransformation of norgestrel (NG), a downstream norgestimate and NGMN metabolite, and found that CYP3A4 and UGT1A1 have a major contribution to the elimination of NG with a combined fm value of 1.	norgestimate	100-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
28502040-0	2017	UGT1A1 polymorphisms with irinotecan-induced toxicities and treatment outcome in Asians with Lung Cancer: a meta-analysis.	Irinotecan	26-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28502040-1	2017	Previous studies of irinotecan pharmacogenetics have shown that the UGT1A1*28 polymorphism has an effect on irinotecan (IRI)-induced toxicities in Caucasians.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28502040-1	2017	Previous studies of irinotecan pharmacogenetics have shown that the UGT1A1*28 polymorphism has an effect on irinotecan (IRI)-induced toxicities in Caucasians.	Irinotecan	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28502040-1	2017	Previous studies of irinotecan pharmacogenetics have shown that the UGT1A1*28 polymorphism has an effect on irinotecan (IRI)-induced toxicities in Caucasians.	Irinotecan	120-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28246004-4	2017	Among them, UGT1A1, UGT1A3, UGT1A6, UGT1A9 and UGT2B7 contributed 95.6% to genistein glucuronidation in human liver, with significant correlation between gene expression of the five UGTs and the glucuronidation of genistein.	Genistein	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28242239-9	2017	Paclitaxel-mediated induction of genes involved in irinotecan metabolism such as Cyp3a11 and Ugt1a1 was TLR4-dependent, while induction of the transporter Mrp2 was TLR4-independent.	Paclitaxel	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
28456840-5	2017	CNSDose (ABCB1, ABCC1, CYP2C19, CYP2D6, UGT1A1) is the only pharmacogenomics test that significantly improved remission (one additional remitting patient in 12 weeks per three genotyped, 95% CI 1.7 to 3.5) and reduced intolerability in an RCT.	cnsdose	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
28242239-9	2017	Paclitaxel-mediated induction of genes involved in irinotecan metabolism such as Cyp3a11 and Ugt1a1 was TLR4-dependent, while induction of the transporter Mrp2 was TLR4-independent.	Irinotecan	51-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
28283555-3	2017	Although neonatal jaundice is mostly benign, excessively high levels of serum bilirubin in a small percentage of newborns can cause bilirubin-induced neurologic dysfunction, potentially leading to permanent brain damage, a condition known as kernicterus Although a large portion of hyperbilirubinemia cases in newborns are associated with hemolytic diseases, we emphasize here the impaired ability of UGT1A1 to eliminate bilirubin that contributes to hyperbilirubinemia-induced neurotoxicity in the developmental stage.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	401-407
27938508-0	2017	Regorafenib Plus FOLFIRI With Irinotecan Dose Escalated According to Uridine Diphosphate Glucuronosyltransferase 1A1 Genotyping in Patients With Metastatic Colorectal Cancer.	regorafenib	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-116
27938508-0	2017	Regorafenib Plus FOLFIRI With Irinotecan Dose Escalated According to Uridine Diphosphate Glucuronosyltransferase 1A1 Genotyping in Patients With Metastatic Colorectal Cancer.	FOLFIRI regimen	17-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-116
27938508-0	2017	Regorafenib Plus FOLFIRI With Irinotecan Dose Escalated According to Uridine Diphosphate Glucuronosyltransferase 1A1 Genotyping in Patients With Metastatic Colorectal Cancer.	Irinotecan	30-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-116
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	regorafenib	27-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	regorafenib	27-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	regorafenib	27-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	FOLFIRI regimen	44-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	FOLFIRI regimen	44-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	FOLFIRI regimen	44-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
28283555-2	2017	Owing to the fact that bilirubin is metabolized solely through glucuronidation by UDP-glucuronosyltransferase (UGT) 1A1, it is now known that immaturity of UGT1A1, in combination with the overproduction of bilirubin during the developmental stage, acts as a bottleneck to bilirubin elimination and predisposes the infant to high total serum bilirubin levels.	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-119
28283555-2	2017	Owing to the fact that bilirubin is metabolized solely through glucuronidation by UDP-glucuronosyltransferase (UGT) 1A1, it is now known that immaturity of UGT1A1, in combination with the overproduction of bilirubin during the developmental stage, acts as a bottleneck to bilirubin elimination and predisposes the infant to high total serum bilirubin levels.	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
28283555-3	2017	Although neonatal jaundice is mostly benign, excessively high levels of serum bilirubin in a small percentage of newborns can cause bilirubin-induced neurologic dysfunction, potentially leading to permanent brain damage, a condition known as kernicterus Although a large portion of hyperbilirubinemia cases in newborns are associated with hemolytic diseases, we emphasize here the impaired ability of UGT1A1 to eliminate bilirubin that contributes to hyperbilirubinemia-induced neurotoxicity in the developmental stage.	Bilirubin	132-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	401-407
28283555-3	2017	Although neonatal jaundice is mostly benign, excessively high levels of serum bilirubin in a small percentage of newborns can cause bilirubin-induced neurologic dysfunction, potentially leading to permanent brain damage, a condition known as kernicterus Although a large portion of hyperbilirubinemia cases in newborns are associated with hemolytic diseases, we emphasize here the impaired ability of UGT1A1 to eliminate bilirubin that contributes to hyperbilirubinemia-induced neurotoxicity in the developmental stage.	Bilirubin	132-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	401-407
28096081-1	2017	Gilbert"s syndrome in humans is derived from a polymorphism (TA repeat) in the hepatic UGT1A1 gene that results in decreased conjugation and increased levels of unconjugated bilirubin.	Bilirubin	174-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
27359323-7	2017	Vitamin A exerted competitive inhibition on the activity of UGT1A1, 2B4, 2B7, and 2B15, and the inhibition kinetic parameters (Ki) were calculated to be 31.1, 16.8, 2.2, and 11.6 muM for UGT1A1, 2B4, 2B7, and 2B15.	Vitamin A	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
27359323-7	2017	Vitamin A exerted competitive inhibition on the activity of UGT1A1, 2B4, 2B7, and 2B15, and the inhibition kinetic parameters (Ki) were calculated to be 31.1, 16.8, 2.2, and 11.6 muM for UGT1A1, 2B4, 2B7, and 2B15.	Vitamin A	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
27977017-1	2017	OBJECTIVE: The objective of our study was to measure the effect of genetic variants of these two enzymes, UGT1A1 and SLCO1B1, in the bilirubin metabolic pathway on the degree of hyperbilirubinemia in a cohort of African-American (AA) infants from our well-baby nursery.	Bilirubin	133-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
27641154-7	2017	Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively.	Fluorouracil	112-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
27641154-7	2017	Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively.	Mercaptopurine	128-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
27641154-7	2017	Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
27832386-3	2017	While polymorphism of UDP-glucuronosyltransferase1A1 (UGT1A1) is involved in detoxification of benzo(a)pyrene-7,8-dihydrodiol(-), a major tobacco carcinogen, the association between UGT1A1 genotype and lung cancer has not been examined.	benzo(a)pyrene 7,8-dihydrodiol	95-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
27832386-3	2017	While polymorphism of UDP-glucuronosyltransferase1A1 (UGT1A1) is involved in detoxification of benzo(a)pyrene-7,8-dihydrodiol(-), a major tobacco carcinogen, the association between UGT1A1 genotype and lung cancer has not been examined.	benzo(a)pyrene 7,8-dihydrodiol	95-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
28065859-7	2017	LAP, PAZ, REG and SOR inhibited UGT1A1-catalysed bilirubin glucuronidation with mean IC50 values ranging from 34nM (REG) to 3734nM (PAZ).	Bilirubin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
28296739-0	2017	UGT1A1*28 relationship with abnormal total bilirubin levels in chronic hepatitis C patients: Outcomes from a case-control study.	Bilirubin	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28346059-5	2017	UGT1A1 rs887829TT (p = 0.002) and CYP1A2 rs762551CC (p = 0.019) resulted as predictive factor of ferritin levels and CYP1A1 rs2606345CA/AA (p = 0.021) and CYP1A2 rs762551AC/CC (p = 0.027) of liver iron concentration.	Iron	197-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
27180825-15	2017	Glucuronidation of belinostat was markedly inhibited by emodin and apigenin (two potent inhibitors of UGT1A1), and by quinidine and diclofenac sodium (two selective inhibitors of UGT2B7).	belinostat	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
28446312-5	2017	Further gene evaluation disclosed a insertion mutation in the (TA)6TAA box, and a missense mutation(G A) at 211 bp of exon 1, corresponding to the deficiency in the bilirubin-conjugating enzyme uridine-diphosphoglucuronosyl transferase1A1 (UGT1A1).	Bilirubin	165-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-238
28446312-5	2017	Further gene evaluation disclosed a insertion mutation in the (TA)6TAA box, and a missense mutation(G A) at 211 bp of exon 1, corresponding to the deficiency in the bilirubin-conjugating enzyme uridine-diphosphoglucuronosyl transferase1A1 (UGT1A1).	Bilirubin	165-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	240-246
28263463-7	2017	The data show that this drug inhibits the enzyme UDP-glucuronosyl transferase-1A1, responsible for conjugating bilirubin with glucuronic acid.	Bilirubin	111-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-81
28263463-7	2017	The data show that this drug inhibits the enzyme UDP-glucuronosyl transferase-1A1, responsible for conjugating bilirubin with glucuronic acid.	Glucuronic Acid	126-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-81
28338110-3	2017	The UGT1A1 promoter (TA) repeats variants are documented of being involved in abnormally elevated bilirubin levels.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
28338110-4	2017	The aim of the present study is to analyze the impact of UGT1A1 promoter variants on bilirubin levels in Romanian patients clinically supected with GS.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
28296739-11	2017	Total bilirubin increase was noticed according to thymine-adenine repeats in genotypes (P &lt; 0.001), and the TB greater than 1 mg/dL group had more UGT1A1*28 subjects than in the group with TB values &lt;1 mg/dL (18.3 vs 5.3; P &lt; 0.001).	Bilirubin	111-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
28296739-13	2017	Among patients with increased TB levels, the frequency of UGT1A1*28 is higher than those with normal TB.	Bilirubin	30-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
28296739-13	2017	Among patients with increased TB levels, the frequency of UGT1A1*28 is higher than those with normal TB.	Bilirubin	101-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
28278081-0	2017	Correlative analysis of plasma SN-38 levels and DPD activity with outcomes of FOLFIRI regimen for metastatic colorectal cancer with UGT1A1 *28 and *6 wild type and its implication for individualized chemotherapy.	Irinotecan	31-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
28278081-1	2017	It remains uncertain whether there is an correlation between clinical pharmacokinetic parameters and outcomes for metastatic colorectal cancer especially with UGT1A1 *28 and *6 wild type (*1/*1-*1/*1) for serious events associated with Irinotecan are largely excluded.	Irinotecan	236-246	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
28278081-2	2017	This study retrospectively analyzed the relationship between Irinotecan metabolite levels and outcomes of UGT1A1 *1/*1-*1/*1 genotype arrangement.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
28278081-8	2017	Therefore, plasma SN-38 levels is related to outcomes for UGT1A1 *1/*1-*1/*1 genotype, to improve efficacy, patients with CSN-38 1.5 h lower than 50.24 ng/ml, CPT-11 dosage could be added in next chemmotherapy on SN-38 plasma level monitoring.	Irinotecan	18-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
27915055-7	2017	The results indicated that UGT1A1 and UGT1A9 were the main isoforms involved in the formation of isofraxidin-7-O-glucuronide.	isofraxidin-7-o-glucuronide	97-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
28296739-4	2017	Our aim was to assess UGT1A1 genotypes" frequency in chronic hepatitis C (CHC) patients and correlate with total bilirubin (TB).	Bilirubin	113-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
28296739-4	2017	Our aim was to assess UGT1A1 genotypes" frequency in chronic hepatitis C (CHC) patients and correlate with total bilirubin (TB).	Bilirubin	124-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
28280378-0	2017	UGT1A1 polymorphisms in cancer: impact on irinotecan treatment.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	175-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	175-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	182-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	182-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	233-243	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	233-243	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-4	2017	Many association studies and meta-analyses have demonstrated the contribution of UGT1A1*28 and UGT1A1*6 polymorphisms to the toxicities caused by irinotecan-based therapy.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
28280378-4	2017	Many association studies and meta-analyses have demonstrated the contribution of UGT1A1*28 and UGT1A1*6 polymorphisms to the toxicities caused by irinotecan-based therapy.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
28131654-2	2017	We investigated whether the polymorphisms of UGT1A1 and UGT1A3 played an important role in the disposition of the drug after oral administration of febuxostat tablet in Chinese subjects.	Febuxostat	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
27507617-1	2017	Purpose:UGT1A1*28 confers a higher risk of toxicity in patients treated with irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
27507617-8	2017	Changes in the AUCs of irinotecan and SN-38 associated with bevacizumab treatment were marginal.Conclusions: The MTD of irinotecan in FOLFIRI plus bevacizumab is 310 mg/m2 for UGT1A1 *1/*1 patients and 260 mg/m2 for *1/*28 patients.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
28173214-0	2017	UGT1A1 polymorphism as a prognostic indicator of stage I ovarian clear cell carcinoma patients treated with irinotecan.	Irinotecan	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28173214-1	2017	We investigated whether UGT1A1 polymorphisms are associated with the prognosis of ovarian cancer patients treated with irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28173214-7	2017	We conclude that UGT1A1 polymorphisms have the potential to be a prognostic marker of irinotecan treatment.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
28017536-5	2017	Glucuronidation of a carboxylate residue is catalyzed by UDP-glucuronosyltransferase 1A and 2B isoforms.	carboxylate	21-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-94
28367249-0	2017	Predictive Value of UGT1A1*28 Polymorphism In Irinotecan-based Chemotherapy.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28367249-1	2017	The UGT1A1*28 polymorphism was suggested to be significantly connected with irinotecan-induced toxicity and response to chemotherapy.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
28367249-3	2017	Hence we carried out a meta-analysis to investigate the effect of UGT1A1*28 polymorphism on severe diarrhea, neutropenia, and response of patients who had undergone irinotecan-based chemotherapy.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
28367249-10	2017	Our data showed that the UGT1A1*28 polymorphism had a significant relationship with toxicity and response to irinotecan-based chemotherapy.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
27654129-3	2017	Dose escalation of irinotecan was performed according to the results of UGT1A1 genotyping in all patients.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
29956901-11	2017	CONCLUSION: SXD could significantly reduce irinotecan-induced hematological and gastrointestinaltoxicities in UGT1A1*28 or *6 variant patients (high risk group), while this treatment didn"t affect clinicalresponse of chemotherapy.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
29098099-0	2017	Life-Threatening Irinotecan-Induced Toxicity in an Adult Patient with Alveolar Rhabdomyosarcoma: The Role of a UGT1A1 Polymorphism.	Irinotecan	17-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-67
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
29098099-8	2017	Physician must be aware of the potential hematological (mainly neutropenia and infectious disease) and digestive (mainly diarrhea) toxicities caused by irinotecan and especially when the patient presents a UGT1A1 *28 homozygous allele.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	206-212
28395759-2	2017	Patients were stratified by their pharmacogenetic/phenotypic status: the irinotecan dose was adjusted according to the number of TA tandem repeats in the UGT1A1 promoter, while the 5-fluorouracil (5-FU) dose was initially adjusted according to dihydropyrimidine dehydrogenase (DPD) activity at initial screening (5-FUODPM Tox) followed by PK-guided dose optimization (5-FUODPM Protocol).	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
28952244-2	2017	Therefore, changes in UGT1A1 expression/functional can not only cause adverse clinical drug/herbs-drug interactions, but also lead to metabolic disorder of endogenous substances, causing high blood bilirubin, bilirubin encephalopathy and liver injury, as well as other side effects.	Bilirubin	198-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
28952244-2	2017	Therefore, changes in UGT1A1 expression/functional can not only cause adverse clinical drug/herbs-drug interactions, but also lead to metabolic disorder of endogenous substances, causing high blood bilirubin, bilirubin encephalopathy and liver injury, as well as other side effects.	Bilirubin	209-218	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
28952244-4	2017	This article would summarize the advances in research on drug metabolism and toxicology in domestic and foreign literature, and investigate the regulatory effects of different types of traditional Chinese medicine(TCM) ingredients(such as flavonoids, coumarins, alkaloids) on UGT1A1 expression and activity, including inhibitory effect of TCM chemical ingredients on UGT1A1 and effect of TCM chemical ingredients on UGT1A1.	Alkaloids	262-271	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	276-282
28098838-0	2017	Role of UDP-Glucuronosyltransferase 1A1 in the Metabolism and Pharmacokinetics of Silymarin Flavonolignans in Patients with HCV and NAFLD.	Silymarin	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
28098838-0	2017	Role of UDP-Glucuronosyltransferase 1A1 in the Metabolism and Pharmacokinetics of Silymarin Flavonolignans in Patients with HCV and NAFLD.	Flavonolignans	92-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	Silybin	164-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	Silybin	175-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	Silybin	183-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	Silybin	194-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	flavonolignan glucuronide	270-295	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	Silybin	413-415	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-3	2017	The aims of this investigation were: (1) to determine the association of UGT1A1*28 polymorphism with the area under the plasma concentration-time curves (AUCs) for silybin A (SA) and silybin B (SB); (2) to evaluate the effect of UGT1A1*28 polymorphism on the profile of flavonolignan glucuronide conjugates found in the plasma; and (3) to investigate the role of UGT1A1 enzyme kinetics on the pharmacokinetics of SA and SB.	Silybin	420-422	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28098838-6	2017	In contrast, an increase in the proportion of sulfated flavonolignan conjugates in plasma was observed in subjects with UGT1A1*28/*28 genotype compared to subjects carrying wild type alleles.	Flavonolignans	55-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
28098838-7	2017	Differences in SA and SB in vitro intrinsic clearance estimates for UGTIA1 correlated inversely with SA and SB exposures observed in vivo indicating a major role for UGT1A1 in silymarin metabolism.	Silymarin	176-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
28098838-8	2017	In addition, a significant difference in the metabolic ratio observed between patients with NAFLD and HCV suggests that any effect of UGT1A1 polymorphism may be obscured by a greater effect of liver disease on the pharmacokinetics of silymarin.	Silymarin	234-243	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
28399191-10	2017	The UGT1A1*28 polymorphism was detected more often among neonates with elevated bilirubin.	Bilirubin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
27943244-1	2017	OBJECTIVE: The present study was undertaken to investigate the genotype and allele frequencies of the variants in the four bilirubin metabolism genes (UGT1A1, OATP2, HMOX1, and BLVRA) and their association with hyperbilirubinemia.	Bilirubin	123-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
27654129-7	2017	FOLFIRI plus bevacizumab as a first-line chemotherapy may achieve effective disease control and be safe in patients with mCRC and hyperbilirubinemia based on UGT1A1 genotyping.	FOLFIRI regimen	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
27503581-5	2017	Both UGT1A1*6 and *28 were reliably demonstrated to be risk factors for irinotecan-induced neutropenia, with tests for both polymorphisms potentially being particularly useful in Asian cancer patients.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
27840292-9	2017	Metabolism and transport of both HT and FA were curtailed by the organic acid lactate owing to a reduction of UGT1A1 protein levels.	organic acid lactate	65-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
27908259-1	2017	BACKGROUND: Bilirubin is a toxic waste product of metabolism, eliminated mainly through UGT1A1 mediated conjugation to mono- and di-glucuronides.	Bilirubin	12-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
27908259-1	2017	BACKGROUND: Bilirubin is a toxic waste product of metabolism, eliminated mainly through UGT1A1 mediated conjugation to mono- and di-glucuronides.	mono- and di-glucuronides	119-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
27908259-8	2017	The Km and Vmax values for total bilirubin glucuronide formations were determined to be 0.05 +- 0.01 muM and 181.9 +- 5.3 pmol/min/mg-protein, respectively, in human recombinant UGT1A1, and 0.23 +- 0.05 muM and 875 +- 45 pmol/min/mg protein in human liver microsomes (HLM).	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	178-184
27908259-8	2017	The Km and Vmax values for total bilirubin glucuronide formations were determined to be 0.05 +- 0.01 muM and 181.9 +- 5.3 pmol/min/mg-protein, respectively, in human recombinant UGT1A1, and 0.23 +- 0.05 muM and 875 +- 45 pmol/min/mg protein in human liver microsomes (HLM).	Glucuronides	43-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	178-184
27704169-1	2017	PURPOSE: Complete or partial inactivity of UGT1A1, the unique enzyme responsible for bilirubin glucuronidation, is commonly associated with hyperbilirubinemia.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
28951772-0	2017	Serum Bilirubin Levels and Promoter Variations in HMOX1 and UGT1A1 Genes in Patients with Fabry Disease.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
28951772-7	2017	However, the presence of the TA7 allele UGT1A1 gene promoter, responsible for higher systemic bilirubin levels, was associated with a twofold lower risk of manifestation of FD (OR = 0.51, 95% CI = 0.27-0.97, p = 0.038).	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
27967321-0	2017	The impact of the UGT1A1*60 allele on bilirubin serum concentrations.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
27967321-2	2017	MATERIALS &amp; METHODS: Retrospective review of clinically obtained serum bilirubin concentrations in pediatric patients to evaluate the association of the UGT1A1 -3279T&gt;G (*60) variant with bilirubin concentrations and assessed linkage disequilibrium of the UGT1A1 -3279T&gt;G (*60) and A(TA)7TAA (*28) variants.	Bilirubin	195-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
26999266-13	2017	Breast mRNA expression of UGTs capable of glucuronidating bisphenol-A was highest for UGT1A1, followed by UGT2B4, UGT1A9, UGT1A10, UGT2B7 and UGT2B15.	bisphenol A	58-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
27967321-4	2017	Total bilirubin concentration was lower in patients homozygous for the UGT1A1 -3279T&gt;G (*60/*60) variant than in patients homozygous for the UGT1A1 A(TA)7TAA (*28/*28) variant (p &lt; 0.01).	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
27967321-4	2017	Total bilirubin concentration was lower in patients homozygous for the UGT1A1 -3279T&gt;G (*60/*60) variant than in patients homozygous for the UGT1A1 A(TA)7TAA (*28/*28) variant (p &lt; 0.01).	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
27883280-0	2017	Phase I study of irinotecan for previously treated lung cancer patients with the UGT1A1*28 or *6 polymorphism: Results of the Lung Oncology Group in Kyushu (LOGIK1004A).	Irinotecan	17-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-90
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-98
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-90
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-98
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
27883280-2	2017	This study was conducted to determine the maximum tolerated dose (MTD) of irinotecan chemotherapy according to the UGT1A1 genotype in previously treated lung cancer patients with the UGT1A1 *28 or UGT1A1 *6 polymorphism.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
27883280-2	2017	This study was conducted to determine the maximum tolerated dose (MTD) of irinotecan chemotherapy according to the UGT1A1 genotype in previously treated lung cancer patients with the UGT1A1 *28 or UGT1A1 *6 polymorphism.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-189
27883280-2	2017	This study was conducted to determine the maximum tolerated dose (MTD) of irinotecan chemotherapy according to the UGT1A1 genotype in previously treated lung cancer patients with the UGT1A1 *28 or UGT1A1 *6 polymorphism.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-189
27883280-10	2017	CONCLUSIONS: The MTD of irinotecan for previously treated lung cancer patients that are heterozygous for the UGT1A1 * 28 or UGT1A1 * 6 gene polymorphism is 60 mg/m2 .	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
27883280-10	2017	CONCLUSIONS: The MTD of irinotecan for previously treated lung cancer patients that are heterozygous for the UGT1A1 * 28 or UGT1A1 * 6 gene polymorphism is 60 mg/m2 .	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
26999266-14	2017	Bisphenol-A glucuronidation was over 10-fold lower in breast tissues with the UGT1A1*28 allele compared with tissues without this allele (p = 0.006).	bis(4-hydroxyphenyl)sulfone	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
27704562-3	2016	Since raltegravir is eliminated mainly by metabolism via an UDP-glucuronosyltransferase (UGT) 1 A1-mediated glucuronidation pathway, co-administration of UGT1A1 inducers may alter plasma levels of raltegravir.	Raltegravir Potassium	6-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-98
27704562-3	2016	Since raltegravir is eliminated mainly by metabolism via an UDP-glucuronosyltransferase (UGT) 1 A1-mediated glucuronidation pathway, co-administration of UGT1A1 inducers may alter plasma levels of raltegravir.	Raltegravir Potassium	6-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
27704562-3	2016	Since raltegravir is eliminated mainly by metabolism via an UDP-glucuronosyltransferase (UGT) 1 A1-mediated glucuronidation pathway, co-administration of UGT1A1 inducers may alter plasma levels of raltegravir.	Raltegravir Potassium	197-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-98
27704562-3	2016	Since raltegravir is eliminated mainly by metabolism via an UDP-glucuronosyltransferase (UGT) 1 A1-mediated glucuronidation pathway, co-administration of UGT1A1 inducers may alter plasma levels of raltegravir.	Raltegravir Potassium	197-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
27696440-7	2016	Since raltegravir is eliminated mainly by metabolism via a uridine diphosphate glucuronosyltransferase (UGT) 1A1-mediated glucuronidation pathway, co-administration of UGT1A1 inhibitors may increase the plasma levels of q.d.	Raltegravir Potassium	6-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-112
28933122-0	2016	[Hepatotoxicity of emodin based on UGT1A1 enzyme-mediated bilirubin in liver microsomes].	Bilirubin	58-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
27696440-7	2016	Since raltegravir is eliminated mainly by metabolism via a uridine diphosphate glucuronosyltransferase (UGT) 1A1-mediated glucuronidation pathway, co-administration of UGT1A1 inhibitors may increase the plasma levels of q.d.	Raltegravir Potassium	6-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	168-174
28933122-1	2016	To study the hepatotoxicity of emodin based on bilirubin metabolism mediated by glucuronidation of UGT1A1 enzyme.	Bilirubin	47-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
30550693-3	2016	Recent pharmacogenetic studies on irinotecan have revealed the impact of UGT1A1 polymorphisms on severe adverse effects.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
27832172-4	2016	Screening assays with 12 human expressed UGT enzymes and chemical-inhibition assays demonstrated that glucuronide formation was almost exclusively catalyzed by UGT1A1, UGT1A6, and UGT1A9.	Glucuronides	102-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
27832172-7	2016	In conclusion, UGT1A1, UGT1A6, and UGT1A9 were the chief contributors to the regioselective glucuronidation of diosmetin and chrysoeriol in the liver.	diosmetin	111-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
27832172-7	2016	In conclusion, UGT1A1, UGT1A6, and UGT1A9 were the chief contributors to the regioselective glucuronidation of diosmetin and chrysoeriol in the liver.	chrysoeriol	125-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
27176228-0	2016	Human UDP-Glucuronosyltransferases 1A1, 1A3, 1A9, 2B4 and 2B7 are Inhibited by Diethylstilbestrol.	Diethylstilbestrol	79-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
27176228-4	2016	DES (10 muM) could decrease activities of UGT1A1, 1A3, 1A9, 2B4 and 2B7 in catalysing 4-methylumbelliferone (4-Mu) glucuronidation.	Diethylstilbestrol	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
27176228-4	2016	DES (10 muM) could decrease activities of UGT1A1, 1A3, 1A9, 2B4 and 2B7 in catalysing 4-methylumbelliferone (4-Mu) glucuronidation.	Hymecromone	86-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
27895797-4	2016	The promoter (-1000 bp) and exon 1 regions of UDP glucuronosyltransferase family 1 member A complex locus (UGT1A1) gene family members UGT1A1, UGT1A7 and UGT1A9 were sequenced, and comprehensive analysis of their genetic polymorphisms was performed to determine the association between inherited genetic variations and irinotecan-induced toxicity.	Irinotecan	319-329	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
27895797-6	2016	The results of the present study revealed that UGT1A1*6 and UGT1A7*3 are risk factors for irinotecan-induced severe neutropenia, and UGT1A9*1b is associated with severe diarrhea.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
27899892-5	2016	We found a statistically significant increase (nominal p &lt; 0.05) in the expression of UGT1A1, UGT1A3, UGT1A4, UGT1A5, UGT1A6, UGT2B7, and UGT2B17, as well as glucuronidation activities of serotonin, testosterone, and vorinostat during the first 25 years of life.	Serotonin	191-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
27899892-5	2016	We found a statistically significant increase (nominal p &lt; 0.05) in the expression of UGT1A1, UGT1A3, UGT1A4, UGT1A5, UGT1A6, UGT2B7, and UGT2B17, as well as glucuronidation activities of serotonin, testosterone, and vorinostat during the first 25 years of life.	Testosterone	202-214	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
27899892-5	2016	We found a statistically significant increase (nominal p &lt; 0.05) in the expression of UGT1A1, UGT1A3, UGT1A4, UGT1A5, UGT1A6, UGT2B7, and UGT2B17, as well as glucuronidation activities of serotonin, testosterone, and vorinostat during the first 25 years of life.	Vorinostat	220-230	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
27781231-4	2016	The control cells were treated with 10 mM acetaminophen without genistein to compare with the effects of the combination of acetaminophen and genistein on the expression of UGT1A1, 1A6 and 1A9, Nrf2 and Keap1 mRNAs, as well as the expression of Nrf2 and Keap1 proteins, which were tested by western blotting.	Acetaminophen	124-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179
27781231-4	2016	The control cells were treated with 10 mM acetaminophen without genistein to compare with the effects of the combination of acetaminophen and genistein on the expression of UGT1A1, 1A6 and 1A9, Nrf2 and Keap1 mRNAs, as well as the expression of Nrf2 and Keap1 proteins, which were tested by western blotting.	Genistein	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179
27895797-0	2016	UGT1A1*6, UGT1A7*3 and UGT1A9*1b polymorphisms are predictive markers for severe toxicity in patients with metastatic gastrointestinal cancer treated with irinotecan-based regimens.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
27895797-4	2016	The promoter (-1000 bp) and exon 1 regions of UDP glucuronosyltransferase family 1 member A complex locus (UGT1A1) gene family members UGT1A1, UGT1A7 and UGT1A9 were sequenced, and comprehensive analysis of their genetic polymorphisms was performed to determine the association between inherited genetic variations and irinotecan-induced toxicity.	Irinotecan	319-329	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
30550693-4	2016	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
30550693-4	2016	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
30550693-5	2016	For patients showing homozygosity for UGT1A1*28, *6 or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
30550693-5	2016	For patients showing homozygosity for UGT1A1*28, *6 or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
27695274-7	2016	Both UGT1A1 and UGT2B7 were inhibited by the ethanol and aqueous extracts with IC50 values ranging between 9.59-22.76 mug/mL and 110.71-526.65 mug/Ml, respectively.	Ethanol	45-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
27676153-6	2016	Fusidic acid also inhibited UGT1A1-catalyzed beta-estradiol glucuronidation activity in human liver microsomes with an IC50 value of 16 muM.	Fusidic Acid	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
27676153-6	2016	Fusidic acid also inhibited UGT1A1-catalyzed beta-estradiol glucuronidation activity in human liver microsomes with an IC50 value of 16 muM.	Estradiol	45-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
27676153-9	2016	The magnitudes of in vivo interaction (R values) resulting from the inhibition of OATP1B1, UGT1A1, NTCP, and BSEP transport were ~1.9-2.6, 1.1-1.2, 1.0-1.1, and 1.4-1.7, respectively, which are indicative of some degree of inherent toxicity risk, particularly via inhibition of OATP and BSEP.	periodate-oxidized adenosine 5'-triphosphate	82-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
27708529-0	2016	Imatinib-induced hyperbilirubinemia with UGT1A1 (*28) promoter polymorphism: first case series in patients with gastrointestinal stromal tumor.	Imatinib Mesylate	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
27708529-2	2016	Severe hepatotoxicity associated with imatinib is rare, and relationship to polymorphism of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) expression and related frequency of hyperbilirubinemia or toxicity are not well known.	Imatinib Mesylate	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
27708529-8	2016	This association is also timely due to recent FDA requirement for testing UGT1A1 polymorphism for nilotinib, another TKI.	nilotinib	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
27767376-6	2016	Although pharmacogenomic studies for HDIs are scarce, available data indicate that therapy with belinostat (UGT1A1), romidepsin (ABCB1), vorinostat (UGT2B17) or VPA (UGT1A6) could be optimized by upfront genotyping.	belinostat	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
26935006-2	2016	Atazanavir (ATV) inhibits UDP-glucuronosyl-transferase 1A1 (UGT1A1), thus increasing unconjugated bilirubin levels.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-58
26935006-2	2016	Atazanavir (ATV) inhibits UDP-glucuronosyl-transferase 1A1 (UGT1A1), thus increasing unconjugated bilirubin levels.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
26935006-2	2016	Atazanavir (ATV) inhibits UDP-glucuronosyl-transferase 1A1 (UGT1A1), thus increasing unconjugated bilirubin levels.	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-58
26935006-2	2016	Atazanavir (ATV) inhibits UDP-glucuronosyl-transferase 1A1 (UGT1A1), thus increasing unconjugated bilirubin levels.	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
26935006-2	2016	Atazanavir (ATV) inhibits UDP-glucuronosyl-transferase 1A1 (UGT1A1), thus increasing unconjugated bilirubin levels.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-58
26935006-2	2016	Atazanavir (ATV) inhibits UDP-glucuronosyl-transferase 1A1 (UGT1A1), thus increasing unconjugated bilirubin levels.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
27695274-9	2016	Xanthorrhizol was the better inhibitor of UGT1A1 (IC50 11.30 +- 0.27 muM) as compared to UGT2B7 while curcumene did not show any inhibition.	xanthorrhizol	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
27116457-4	2016	RESULTS: After adjustment of the tests by the UGT1A1*28 genotype and correction for multiple testing, the A allele of NR1I2-rs10934498 was associated with a decreased exposition and an increased degradation of SN-38, the active metabolite (p = 0.009 and p = 0.017, respectively).	Irinotecan	210-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
27372715-6	2016	UDP-glucuronyltransferase (UGT) initial activity screening showed that UGT1A1, UGT1A8, UGT1A9, UGT1A10, UGT2B4, UGT2B7, UGT2B15, and UGT2B17 formed desomorphine glucuronide.	desomorphine glucuronide	148-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
27428458-8	2016	Psoralidin showed potent and noncompetitive inhibition against UGT1A1, UGT1A7, CYP1A2 and CYP2C8 with IC50 values of 6.12, 0.38, 1.81, 0.28muM, respectively.	psoralidin	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
26833852-3	2016	The results showed that most model flavonoids (from a total of 13) were mainly metabolized into glucuronides in the MDCKII-UGT1A1/MRP2 cells and the glucuronides were rapidly excreted.	Flavonoids	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
27746618-10	2016	The mutant, but not wild type or heterozygous genotype of SNPs (rs6742078 and rs887829) in UGT1A1 gene, was associated with significantly higher levels of bilirubin.	Bilirubin	155-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
27746618-11	2016	CONCLUSIONS: Higher incidence of pigment stones in South Indians could be due to raised serum bilirubin levels that may be ascribed to variant in the UGT1A1 gene involved in glucuronidation of free bilirubin.	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
27746618-11	2016	CONCLUSIONS: Higher incidence of pigment stones in South Indians could be due to raised serum bilirubin levels that may be ascribed to variant in the UGT1A1 gene involved in glucuronidation of free bilirubin.	Bilirubin	198-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
27565905-2	2016	We report a case in which gefitinib- and elrotinib-induced severe hepatotoxicity arose in a patient with the uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) and cytochrome p450 3A5 (CYP3A5) poor metabolizer phenotypes.	Gefitinib	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-164
27565905-2	2016	We report a case in which gefitinib- and elrotinib-induced severe hepatotoxicity arose in a patient with the uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) and cytochrome p450 3A5 (CYP3A5) poor metabolizer phenotypes.	Gefitinib	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
27565905-2	2016	We report a case in which gefitinib- and elrotinib-induced severe hepatotoxicity arose in a patient with the uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) and cytochrome p450 3A5 (CYP3A5) poor metabolizer phenotypes.	elrotinib	41-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-164
27565905-2	2016	We report a case in which gefitinib- and elrotinib-induced severe hepatotoxicity arose in a patient with the uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) and cytochrome p450 3A5 (CYP3A5) poor metabolizer phenotypes.	elrotinib	41-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
26833852-3	2016	The results showed that most model flavonoids (from a total of 13) were mainly metabolized into glucuronides in the MDCKII-UGT1A1/MRP2 cells and the glucuronides were rapidly excreted.	Glucuronides	96-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
26833852-3	2016	The results showed that most model flavonoids (from a total of 13) were mainly metabolized into glucuronides in the MDCKII-UGT1A1/MRP2 cells and the glucuronides were rapidly excreted.	Glucuronides	149-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
26833852-6	2016	Maximal velocity of glucuronide production MDCK-MRP2/UGT1A1 cells showed a fairly good correlation (R(2) &gt;0.8) with those derived using UGT1A1 microsomes, but other kinetic parameters (e.g., Km ) did not correlate.	Glucuronides	20-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
26833852-6	2016	Maximal velocity of glucuronide production MDCK-MRP2/UGT1A1 cells showed a fairly good correlation (R(2) &gt;0.8) with those derived using UGT1A1 microsomes, but other kinetic parameters (e.g., Km ) did not correlate.	Glucuronides	20-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
27533851-0	2016	Polymorphisms in SLCO1B1 and UGT1A1 are associated with sorafenib-induced toxicity.	Sorafenib	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
27533851-7	2016	CONCLUSION: Polymorphisms in SLCO1B1 and UGT1A1 are associated with several different sorafenib side effects.	Sorafenib	86-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
28920386-7	2016	In conclusion, the results indicated that chloroform extract showed different inhibitory effects on UGTs and UGT1A1 activity, which may be one of the mechanisms of liver injury induced by Genkwa Flos.	Chloroform	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
28920386-0	2016	[In vitro effects of Genkwa Flos chloroform extract on activity of human liver microsomes UGTs and UGT1A1].	Chloroform	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
26626330-10	2016	Both compounds induced several drug metabolizing genes (including CYP2B6, CYP3A4 and UGT1A1), mediated by CAR activation in Nevirapine and PXR in Ritonavir.	Nevirapine	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
28920386-2	2016	In the present study, 4-nitrophenol(4-NP) and beta-estradiol were elected as substrates to determine activities of UGTs and UGT1A1 by UV and HPLC.	4-nitrophenol	22-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
28920386-2	2016	In the present study, 4-nitrophenol(4-NP) and beta-estradiol were elected as substrates to determine activities of UGTs and UGT1A1 by UV and HPLC.	4-nonylphenol	36-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
28920386-2	2016	In the present study, 4-nitrophenol(4-NP) and beta-estradiol were elected as substrates to determine activities of UGTs and UGT1A1 by UV and HPLC.	Estradiol	46-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
27529203-3	2016	We also predicted potential dietary supplement-drug interactions for beta-cryptoxanthin via UGT1A1 inhibition.	Beta-Cryptoxanthin	69-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
27529203-5	2016	beta-Cryptoxanthin mildly inhibited UGT1A1, UGT1A3, and UGT1A4, with IC50 values of 18.8 +- 2.07, 28.3 +- 4.40 and 34.9 +- 5.98 muM, respectively.	Beta-Cryptoxanthin	0-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
27529203-6	2016	Canthaxanthin weakly inhibited UGT1A1 and UGT1A3, with IC50 values of 38.5 +- 4.65 and 41.2 +- 3.14 muM, respectively; and lutein inhibited UGT1A1 and UGT1A4, with IC50 values of 45.5 +- 4.01 and 28.7 +- 3.79 muM, respectively.	Canthaxanthin	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
27529203-6	2016	Canthaxanthin weakly inhibited UGT1A1 and UGT1A3, with IC50 values of 38.5 +- 4.65 and 41.2 +- 3.14 muM, respectively; and lutein inhibited UGT1A1 and UGT1A4, with IC50 values of 45.5 +- 4.01 and 28.7 +- 3.79 muM, respectively.	Canthaxanthin	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
27529203-7	2016	Among the tested xanthophyll-UGT pairs, beta-cryptoxanthin showed the strongest competitive inhibition of UGT1A1 (Ki, 12.2 +- 0.985 muM).	Beta-Cryptoxanthin	40-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
27529203-8	2016	In addition, we predicted the risk of UGT1A1 inhibition in vivo using the reported maximum plasma concentration after oral administration of beta-cryptoxanthin in humans.	Beta-Cryptoxanthin	141-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
26626330-10	2016	Both compounds induced several drug metabolizing genes (including CYP2B6, CYP3A4 and UGT1A1), mediated by CAR activation in Nevirapine and PXR in Ritonavir.	Ritonavir	146-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
27197997-6	2016	Activation of CAR and PXR in cells treated with a high dose of CITCO [6-(4-chlorophenyl)-imidazo(2,1-b)thiazole-5-carbaldehyde] or cotreated with rifampicin and tetracycline resulted in synergistic enhancement of CYP3A4, but not CYP2B6, CYP2C9, or UGT1A1, mRNA expression in HepTR/hCAR/hPXR cells.	6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	248-254
27197997-6	2016	Activation of CAR and PXR in cells treated with a high dose of CITCO [6-(4-chlorophenyl)-imidazo(2,1-b)thiazole-5-carbaldehyde] or cotreated with rifampicin and tetracycline resulted in synergistic enhancement of CYP3A4, but not CYP2B6, CYP2C9, or UGT1A1, mRNA expression in HepTR/hCAR/hPXR cells.	6-(4-chlorophenyl)-imidazo(2,1-b)thiazole	70-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	248-254
27325020-6	2016	However, a PGG glucuronide was absent in the UGT1A1 system.	Glucuronides	15-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
26829336-11	2016	Resveratrol was a competitive inhibitor of UGT1A1, UGT1A9 and HLM; quercetin and kaempferol were inhibitors of all transferases under investigation except UGT2B15.	Resveratrol	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
27380166-0	2016	Erratum to: UDP-glucuronosyltransferase 1A1*6 and *28 polymorphisms as indicators of initial dose level of irinotecan to reduce risk of neutropenia in patients receiving FOLFIRI for colorectal cancer.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-43
26710796-0	2016	UDP-glucuronosyltransferase 1A1*6 and *28 polymorphisms as indicators of initial dose level of irinotecan to reduce risk of neutropenia in patients receiving FOLFIRI for colorectal cancer.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
26632033-10	2016	ABT-751 is metabolized by UGT1A8 and to a lesser extent UGT1A4 and UGT1A1.	ABT751	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
27057738-2	2016	We evaluated the role of variations in the bilirubin uridine-5-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1) in unconjugated hyperbilirubinemia development during chemotherapy in pediatric patients with leukemia.	Bilirubin	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
27057738-2	2016	We evaluated the role of variations in the bilirubin uridine-5-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1) in unconjugated hyperbilirubinemia development during chemotherapy in pediatric patients with leukemia.	Uridine Diphosphate	53-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
27057738-3	2016	METHODS: UGT1A1 allelic variations were evaluated in 25 Japanese pediatric leukemia patients with hyperbilirubinemia (peak serum bilirubin concentration 3.57 +- 1.02 mg/dl) and 25 control patients without hyperbilirubinemia (0.92 +- 0.32 mg/dl) by PCR-direct sequencing.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
27220761-0	2016	UGT1A1 gene polymorphism is associated with toxicity and clinical efficacy of irinotecan-based chemotherapy in patients with advanced colorectal cancer.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26739304-0	2016	High Resectability Rate of Initially Unresectable Colorectal Liver Metastases After UGT1A1-Adapted High-Dose Irinotecan Combined with LV5FU2 and Cetuximab: A Multicenter Phase II Study (ERBIFORT).	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
26739304-14	2016	It seemed to be well-tolerated among healthy selected patients thanks to irinotecan dose adaptation according to UGT1A1 pharmacogenomics status.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
27220761-1	2016	OBJECTIVES: To investigate the relationship between uridine diphosphate glucoronosyltransferase 1A1 (UGT1A1)*28/*6 and toxicity and clinical efficacy of irinotecan-based chemotherapy in patients with advanced colorectal cancer (CRC) in Xinjiang Uygur and Han population.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-99
27220761-1	2016	OBJECTIVES: To investigate the relationship between uridine diphosphate glucoronosyltransferase 1A1 (UGT1A1)*28/*6 and toxicity and clinical efficacy of irinotecan-based chemotherapy in patients with advanced colorectal cancer (CRC) in Xinjiang Uygur and Han population.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
27220761-11	2016	CONCLUSION: UGT1A1 gene polymorphism predicts irinotecan-related adverse reactions in advanced CRC patients of Xinjiang Uygur and Han nationality; UGT1A1 gene polymorphism is correlated with efficacy and prognosis in Uygur nationality, but only related to prognosis in Han nationality in irinotecan-based chemotherapy.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
27220761-11	2016	CONCLUSION: UGT1A1 gene polymorphism predicts irinotecan-related adverse reactions in advanced CRC patients of Xinjiang Uygur and Han nationality; UGT1A1 gene polymorphism is correlated with efficacy and prognosis in Uygur nationality, but only related to prognosis in Han nationality in irinotecan-based chemotherapy.	Irinotecan	288-298	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
27220761-11	2016	CONCLUSION: UGT1A1 gene polymorphism predicts irinotecan-related adverse reactions in advanced CRC patients of Xinjiang Uygur and Han nationality; UGT1A1 gene polymorphism is correlated with efficacy and prognosis in Uygur nationality, but only related to prognosis in Han nationality in irinotecan-based chemotherapy.	Irinotecan	288-298	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
27160286-1	2016	PURPOSE: UGT1A1*28/*6 as predictors of severe irinotecan-related diarrhea (SIRD) were duplicated by many studies.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
27029846-8	2016	Concomitant administration of non-ritonavir-boosted atazanavir decreased elvitegravir clearance by 35%, likely due to UDP-glucuronosyl transferase (UGT) 1A1 inhibition.	Ritonavir	34-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-156
27029846-8	2016	Concomitant administration of non-ritonavir-boosted atazanavir decreased elvitegravir clearance by 35%, likely due to UDP-glucuronosyl transferase (UGT) 1A1 inhibition.	Atazanavir Sulfate	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-156
27160286-0	2016	A novel genetic score model of UGT1A1 and TGFB pathway as predictor of severe irinotecan-related diarrhea in metastatic colorectal cancer patients.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
26898568-1	2016	PURPOSE: Dolutegravir (DTG) is primarily metabolized by UGT1A1 with CYP3A as a minor route.	dolutegravir	9-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
27089846-4	2016	The results demonstrated that both tolcapone and entacapone exhibited inhibitory effects on UGT1A1, UGT1A7, UGT1A9 and UGT1A10.	Tolcapone	35-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
27089846-4	2016	The results demonstrated that both tolcapone and entacapone exhibited inhibitory effects on UGT1A1, UGT1A7, UGT1A9 and UGT1A10.	entacapone	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
26862009-0	2016	Impact of UGT1A1 genotype upon toxicities of combination with low-dose irinotecan plus platinum.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
26862009-0	2016	Impact of UGT1A1 genotype upon toxicities of combination with low-dose irinotecan plus platinum.	Platinum	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
26862009-1	2016	AIM: Irinotecan-induced severe toxicities are possibly related to UGT1A1*6 and *28 genotypes.	Irinotecan	5-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
26862009-2	2016	However, the correlation between UGT1A1 polymorphisms and the risk of toxicities induced by low-dose irinotecan plus platinum combination therapy still remains controversial.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26862009-2	2016	However, the correlation between UGT1A1 polymorphisms and the risk of toxicities induced by low-dose irinotecan plus platinum combination therapy still remains controversial.	Platinum	117-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26862009-3	2016	This prospective observational study aimed to examine the correlation between UGT1A1 genotypes and clinical outcomes of low-dose irinotecan (median 60 mg/m(2) , range 25-115 mg/m(2) ) plus platinum in Japanese patients with solid tumors.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
26862009-10	2016	CONCLUSION: UGT1A1 genotype has a major impact on the increased risk of severe hematological toxicities, even in low-dose irinotecan regimens.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
26862009-11	2016	UGT1A1 genotypes are useful biomarkers for predicting severe hematological toxicities in patients treated with irinotecan plus platinum analog.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26862009-11	2016	UGT1A1 genotypes are useful biomarkers for predicting severe hematological toxicities in patients treated with irinotecan plus platinum analog.	Platinum	127-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
27385990-0	2016	Prospective study of the UGT1A1*27 gene polymorphism during irinotecan therapy in patients with lung cancer: Results of Lung Oncology Group in Kyusyu (LOGIK1004B).	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
27385990-2	2016	To evaluate the effect of the UGT1A1*27 polymorphism in irinotecan therapy, we conducted a prospective study.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
27385990-10	2016	In an evaluation of the side effects of irinotecan, patients with UGT1A1*28 and UGT1A1*6 polymorphisms had a higher tendency to experience febrile neutropenia than wild type (25% and 32% vs. 14%).	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
27385990-10	2016	In an evaluation of the side effects of irinotecan, patients with UGT1A1*28 and UGT1A1*6 polymorphisms had a higher tendency to experience febrile neutropenia than wild type (25% and 32% vs. 14%).	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
27089846-5	2016	In contrast to entacapone, tolcapone exhibited more potent inhibitory effects on UGT1A1, UGT1A7, and UGT1A10, while their inhibitory potentials against UGT1A9 were comparable.	Tolcapone	27-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
27089846-6	2016	It is noteworthy that the inhibition constants (Ki) of tolcapone and entacapone against bilirubin-O-glucuronidation in human liver microsomes (HLM) are determined as 0.68muM and 30.82muM, respectively, which means that the inhibition potency of tolcapone on UGT1A1 mediated bilirubin-O-glucuronidation in HLM is much higher than that of entacapone.	Tolcapone	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	258-264
27089846-6	2016	It is noteworthy that the inhibition constants (Ki) of tolcapone and entacapone against bilirubin-O-glucuronidation in human liver microsomes (HLM) are determined as 0.68muM and 30.82muM, respectively, which means that the inhibition potency of tolcapone on UGT1A1 mediated bilirubin-O-glucuronidation in HLM is much higher than that of entacapone.	entacapone	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	258-264
27089846-7	2016	Furthermore, the potential risks of tolcapone or entacapone via inhibition of human UGT1A1 were quantitatively predicted by the ratio of the areas under the plasma drug concentration-time curve (AUC).	Tolcapone	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
27089846-7	2016	Furthermore, the potential risks of tolcapone or entacapone via inhibition of human UGT1A1 were quantitatively predicted by the ratio of the areas under the plasma drug concentration-time curve (AUC).	entacapone	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
27089846-8	2016	The results indicate that tolcapone may result in significant increase in AUC of bilirubin or the drugs primarily metabolized by UGT1A1, while entacapone is unlikely to cause a significant DDI through inhibition of UGT1A1.	Tolcapone	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
27296832-1	2016	BACKGROUND: To investigate the associations between atorvastatin-induced liver injury (AILI) and polymorphisms in eight genes possibly involved in the hepatic metabolism (CYP2C9, CYP2C19, CYP3A4, CYP3A5 and UGT1A1) and membrane transport (ABCB1, ABCG2 and SLCO1B1) of atorvastatin, we genotyped 30 AILI and 414 non-AILI patients recruited at BioBank Japan for 15 single nucleotide polymorphisms (SNPs).	Atorvastatin	52-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	207-213
26898568-1	2016	PURPOSE: Dolutegravir (DTG) is primarily metabolized by UGT1A1 with CYP3A as a minor route.	dolutegravir	23-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
26758854-0	2016	Efflux Transport Characterization of Resveratrol Glucuronides in UDP-Glucuronosyltransferase 1A1 Transfected HeLa Cells: Application of a Cellular Pharmacokinetic Model to Decipher the Contribution of Multidrug Resistance-Associated Protein 4.	resveratrol glucuronides	37-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-96
27323053-7	2016	The serum bilirubin levels seem to be affected by the homozygosity or heterozygosity of the UGT1A1 gene mutation; 211G&gt;A homozygous mutation is an important factor that causes a rise in bilirubin in neonates with unconjugated hyperbilirubinemia.	Bilirubin	10-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
27323053-7	2016	The serum bilirubin levels seem to be affected by the homozygosity or heterozygosity of the UGT1A1 gene mutation; 211G&gt;A homozygous mutation is an important factor that causes a rise in bilirubin in neonates with unconjugated hyperbilirubinemia.	Bilirubin	189-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
29874021-9	2016	The sciadopitysin competitively inhibited the formation of 4-MU-O-glucuronide by UGT1A1, UGT1A3, UGT1A8, and UGT1A10.	4-mu-o-glucuronide	59-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
29874021-10	2016	At the same time, the inhibition of NCHN-O-glucuronidation by UGT1A1 was consistent with the competitive inhibition.	nchn-o	36-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
27099654-7	2016	Phenobarbitone being an inducer of enzyme UDPGT is used as the first line of treatment and is not teratogenic in the low doses used.	Phenobarbital	0-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-47
27122675-1	2016	AIM: To examine the predictive effects of baseline serum bilirubin levels and UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism on response of colorectal cancer to irinotecan-based chemotherapy.	Irinotecan	168-178	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-115
27122675-9	2016	RESULTS: Among the 120 mCRC patients, the serum bilirubin level was significantly different between the UGT1A1*28 wild-type and mutant genotypes.	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
27122675-16	2016	CONCLUSION: CoBil and UGT1A1*28 are both independent biomarkers for predicting the treatment response of mCRC patients to irinotecan-based chemotherapy.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
26417955-1	2016	The antiretroviral protease inhibitor atazanavir inhibits hepatic uridine diphosphate glucuronosyltransferase (UGT) 1A1, thereby preventing the glucuronidation and elimination of bilirubin.	Atazanavir Sulfate	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-119
26417955-1	2016	The antiretroviral protease inhibitor atazanavir inhibits hepatic uridine diphosphate glucuronosyltransferase (UGT) 1A1, thereby preventing the glucuronidation and elimination of bilirubin.	Bilirubin	179-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-119
26417955-3	2016	Risk for bilirubin-related discontinuation is highest among individuals who carry two UGT1A1 decreased function alleles (UGT1A1*28 or *37).	Bilirubin	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
26417955-3	2016	Risk for bilirubin-related discontinuation is highest among individuals who carry two UGT1A1 decreased function alleles (UGT1A1*28 or *37).	Bilirubin	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
26417955-4	2016	We summarize published literature that supports this association and provide recommendations for atazanavir prescribing when UGT1A1 genotype is known (updates at www.pharmgkb.org).	Atazanavir Sulfate	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
26758854-3	2016	Here, we aimed to characterize the efflux transport of resveratrol glucuronides using UGT1A1-overexpressing HeLa cells (HeLa1A1 cells), and to determine the contribution of multidrug resistance-associated protein (MRP) 4 to cellular excretion of the glucuronides.	resveratrol glucuronides	55-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
26758854-3	2016	Here, we aimed to characterize the efflux transport of resveratrol glucuronides using UGT1A1-overexpressing HeLa cells (HeLa1A1 cells), and to determine the contribution of multidrug resistance-associated protein (MRP) 4 to cellular excretion of the glucuronides.	Glucuronides	67-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
27080842-6	2016	Other tests are also commonly performed to address the toxicity of certain anticancer drugs (DPYD-capecitabine, UGT1A1-irinotecan, TPMT 6-mercaptopurine).	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
27461651-2	2016	DPYD*2A/*5A/*9A and UGT1A1 * 6/*28 polymorphisms are related to the toxicity of fluorouracil drugs and irinotecan, respectively.	Fluorouracil	80-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
27461651-2	2016	DPYD*2A/*5A/*9A and UGT1A1 * 6/*28 polymorphisms are related to the toxicity of fluorouracil drugs and irinotecan, respectively.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
26313268-2	2016	Polymorphisms that reduce UGT1A1 function could result in increased belinostat exposure and toxicities.	belinostat	68-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
26313268-10	2016	UGT1A1 polymorphisms were associated with increased systemic belinostat exposure, increased AcK, and increased incidence of toxicities, particularly at doses &gt; 400 mg/m(2) /24 h.	belinostat	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26637161-2	2016	Belinostat is predominantly metabolized by UGT1A1, which is polymorphic.	belinostat	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
26637161-6	2016	This model and subsequent simulations supported additional PK/toxicity and pharmacogenomics/toxicity analyses to suggest a UGT1A1 genotype-based dose adjustment to normalize belinostat exposure and allow for more tolerable therapy.	belinostat	174-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
27034809-6	2016	The presence of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *28 polymorphism is associated with toxicity from irinotecan, although it has not been universally applied.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-67
27034809-6	2016	The presence of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *28 polymorphism is associated with toxicity from irinotecan, although it has not been universally applied.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
26189431-3	2016	The in vitro studies using atazanavir as a selective inhibitor of UGT1A1 and -1A3 indicated that these enzymes contribute ~55% toward the overall glucuronidation pathway.	Atazanavir Sulfate	27-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-81
27025983-6	2016	Dimerization changed the chemical regioselectivity, substrate-binding affinity, and enzymatic activity of UGT1A1 and UGT1A9 in glucuronidation of quercetin.	Quercetin	146-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
27025983-7	2016	These findings provide molecular insights into the consequences of homozygous and heterozygous UGT1A1 and UGT1A9 allozymes expression on quercetin glucuronidation.	Quercetin	137-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
26781906-0	2016	Three-dimensional polyacrylamide gel-based DNA microarray method effectively identifies UDP-glucuronosyltransferase 1A1 gene polymorphisms for the correct diagnosis of Gilbert"s syndrome.	polyacrylamide	18-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-119
26781906-2	2016	The T-3279G mutation in the phenobarbital responsive enhancer module (PBREM), the TA-insertion in the TATA box, creating the A(TA)7TAA motif instead of A(TA)6TAA and the G211A mutation in coding exon 1, particularly in Asian populations, of the human UGT1A1 gene are the three common genotypes found in patients with Gilbert"s syndrome.	Phenobarbital	28-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
26781906-4	2016	In this study, to the best of our knowledge, we established a three-dimensional polyacrylamide gel-based DNA microarray method for the first time, in order to study UGT1A1 gene polymorphisms.	polyacrylamide	80-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
26781906-7	2016	The data from the current study demonstrate that the three-dimensional polyacrylamide gel microarray method has the potential to be applied as a useful, reliable and cost-effective tool to detect the T-3279G, the A(TA)6/7TAA and the G211A mutations of the UGT1A1 gene in patients with hyperbilirubinemia and thereby aid in the diagnosis of Gilbert"s syndrome.	polyacrylamide	71-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	256-262
26146896-2	2016	Indeed, this is the first report that interested in the study of polymorphisms in genes encoded for enzymes involved in the bilirubin metabolism: rs 4149056 of SLCO1B1 and rs4149000 of SLCO1A2 in combination with rs8175347 and rs887829 of UGT1A1 in order to find a correlation between the polymorphisms studied and the presence of gallstones in a population of sickle cell anemia (SCA) pediatric Tunisians.	Bilirubin	124-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	239-245
26857783-4	2016	RESULTS AND CONCLUSION: UGT1A1*6 and UGT1A1*28 polymorphisms were associated with severe neutropenia (p = 0.025, p = 0.022, respectively) but not diarrhea (p = 0.343, p = 0.185, respectively), and ABCB1- 3435C&gt;T polymorphism was not associated with irinotecan induced severe toxicities (p = 0.457, p = 0.161, respectively).	Irinotecan	252-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26857783-4	2016	RESULTS AND CONCLUSION: UGT1A1*6 and UGT1A1*28 polymorphisms were associated with severe neutropenia (p = 0.025, p = 0.022, respectively) but not diarrhea (p = 0.343, p = 0.185, respectively), and ABCB1- 3435C&gt;T polymorphism was not associated with irinotecan induced severe toxicities (p = 0.457, p = 0.161, respectively).	Irinotecan	252-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
26189431-4	2016	Therefore, a clinical study was conducted to assess the potential for drug interaction between pradigastat and probenecid (purported general UGT inhibitor) or atazanavir (selective UGT1A1, -1A3 inhibitor).	pradigastat	95-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-187
26502886-8	2016	In the presence of 50 nM curcumin, the clearance of resveratrol-3-O-glucuronide and resveratrol-3-O-sulfate reduced in both MRP2-overexpressing MDCKII-UGT1A1 cells and Human UGT1A9-overexpressing HeLa cells.	Curcumin	25-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
26502886-8	2016	In the presence of 50 nM curcumin, the clearance of resveratrol-3-O-glucuronide and resveratrol-3-O-sulfate reduced in both MRP2-overexpressing MDCKII-UGT1A1 cells and Human UGT1A9-overexpressing HeLa cells.	resveratrol-4'-O-glucuronide	52-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
26773202-1	2016	Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.	Irinotecan	271-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-85
26773202-1	2016	Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.	Irinotecan	271-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
26773202-1	2016	Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.	Irinotecan	271-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
26773202-3	2016	Belinostat, approved for the treatment of peripheral T-cell lymphoma, is primarily glucuronidated by UGT1A1.	belinostat	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
26502886-8	2016	In the presence of 50 nM curcumin, the clearance of resveratrol-3-O-glucuronide and resveratrol-3-O-sulfate reduced in both MRP2-overexpressing MDCKII-UGT1A1 cells and Human UGT1A9-overexpressing HeLa cells.	Resveratrol-3-O-sulfate	84-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
26773202-4	2016	Recent preclinical and clinical data showed that UGT1A1*28 was associated with reduced glucuronidation in human liver microsomes, while in a retrospective analysis of a Phase I trial with patients receiving belinostat UGT1A1*60 was predominantly associated with increased belinostat plasma concentrations.	belinostat	207-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
26773202-4	2016	Recent preclinical and clinical data showed that UGT1A1*28 was associated with reduced glucuronidation in human liver microsomes, while in a retrospective analysis of a Phase I trial with patients receiving belinostat UGT1A1*60 was predominantly associated with increased belinostat plasma concentrations.	belinostat	207-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	218-224
26773202-4	2016	Recent preclinical and clinical data showed that UGT1A1*28 was associated with reduced glucuronidation in human liver microsomes, while in a retrospective analysis of a Phase I trial with patients receiving belinostat UGT1A1*60 was predominantly associated with increased belinostat plasma concentrations.	belinostat	272-282	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
26830078-0	2016	Correlation of UGT1A1(*)28 and (*)6 polymorphisms with irinotecan-induced neutropenia in Thai colorectal cancer patients.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26547877-5	2016	DPhP and DNOP weakly inhibited the activities of UGT1A1, UGT1A7, and UGT1A8.	dphp	0-4	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
26547877-5	2016	DPhP and DNOP weakly inhibited the activities of UGT1A1, UGT1A7, and UGT1A8.	di-n-octyl phthalate	9-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
26830078-1	2016	UDP-glucuronosyltransferase1A1 (UGT1A1) polymorphisms have been related with irinotecan toxicity.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
26830078-1	2016	UDP-glucuronosyltransferase1A1 (UGT1A1) polymorphisms have been related with irinotecan toxicity.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
26830078-2	2016	The purpose of this study was to determine the associations between UGT1A1(*)28 and (*)6 polymorphisms and irinotecan toxicity in Thai patients with metastatic colorectal cancer.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
26830078-10	2016	Both UGT1A1(*)28 and (*)6 polymorphisms may have an increased risk of irinotecan-induced neutropenia in Thai colorectal cancer patients.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
28868871-2	2016	In the present study, 4-nitrophenol (4-NP) and beta-estradiol were elected as substrates to determine activities of UGTs and UGT1A1 by UV and HPLC, respectively.	4-nitrophenol	22-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
25869015-6	2016	For SN-38 AUC0-24 and the glucuronidation ratio, we replicated UGT1A1*28 and UGT1A1*93.	Irinotecan	4-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
25869015-6	2016	For SN-38 AUC0-24 and the glucuronidation ratio, we replicated UGT1A1*28 and UGT1A1*93.	Irinotecan	4-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
25869015-7	2016	In addition to UGT1A1*28, this study independently validated UGT1A1*93 and SLCO1B1*1b as new predictors of irinotecan neutropenia.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
28868871-2	2016	In the present study, 4-nitrophenol (4-NP) and beta-estradiol were elected as substrates to determine activities of UGTs and UGT1A1 by UV and HPLC, respectively.	4-nitrophenol	37-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
28868871-2	2016	In the present study, 4-nitrophenol (4-NP) and beta-estradiol were elected as substrates to determine activities of UGTs and UGT1A1 by UV and HPLC, respectively.	Estradiol	47-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
26808671-0	2016	Phenotyping of UGT1A1 Activity Using Raltegravir Predicts Pharmacokinetics and Toxicity of Irinotecan in FOLFIRI.	Raltegravir Potassium	37-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26820647-0	2016	Molecular Genetics External Quality Assessment Pilot Scheme for Irinotecan-Related UGT1A1 Genotyping in China.	Irinotecan	64-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
26820647-2	2016	Molecular testing for UGT1A1 genotyping is increasingly required in China for optimum irinotecan administration.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
26808671-0	2016	Phenotyping of UGT1A1 Activity Using Raltegravir Predicts Pharmacokinetics and Toxicity of Irinotecan in FOLFIRI.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26811156-0	2016	Prospective analysis of UGT1A1 promoter polymorphism for irinotecan dose escalation in metastatic colorectal cancer patients treated with bevacizumab plus FOLFIRI as the first-line setting: study protocol for a randomized controlled trial.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26808671-1	2016	BACKGROUND: Irinotecan toxicity correlates with UGT1A1 activity.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
26811156-0	2016	Prospective analysis of UGT1A1 promoter polymorphism for irinotecan dose escalation in metastatic colorectal cancer patients treated with bevacizumab plus FOLFIRI as the first-line setting: study protocol for a randomized controlled trial.	FOLFIRI regimen	155-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26098842-2	2016	This study evaluates the cost-effectiveness of UGT1A1 genotyping in patients with metastatic colorectal cancer undergoing irinotecan-based chemotherapy compared to no testing from the perspective of the German statutory health insurance.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
26811156-3	2016	Therefore, we plan to explore the effect of the genetic polymorphism of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) for irinotecan detoxification in mCRC patients.	Irinotecan	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-119
26811156-3	2016	Therefore, we plan to explore the effect of the genetic polymorphism of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) for irinotecan detoxification in mCRC patients.	Irinotecan	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
26811156-6	2016	METHODS/DESIGN: This trial is a prospective, multicenter, randomized clinical trial comparing UGT1A1 promoter polymorphism for irinotecan dose escalation in mCRC patients administered with bevacizumab plus FOLFIRI as the first-line setting.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
26811156-8	2016	The study group receive a biweekly FOLFIRI regimen, with irinotecan dose escalation based on UGT1A1 genotyping; whereas the control group receive the conventional biweekly FOLFIRI regimen without UGT1A1 genotyping.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
26811156-10	2016	DISCUSSION: Patients with mCRC undergoing UGT1A1 genotyping may receive escalated doses of irinotecan for a potentially more favorable clinical response and outcome, in addition to comparable toxicities.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
26549688-6	2016	RT-PCR analysis showed that PXR SUMOylation in presence of rifampicin also enhances the endogenous expression levels of key PXR-regulated genes like CYP3A4, CYP2C9, MDR1 and UGT1A1.	Rifampin	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
26872008-0	2016	Phase II and UGT1A1 Polymorphism Study of Two Different Irinotecan Dosages Combined with Cisplatin as First-Line Therapy for Advanced Gastric Cancer.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
27725437-2	2016	Trovafloxacin is mainly metabolized to its acyl-glucuronide by uridine 5"-diphosphate (UDP)-glucuronosyltransferase (UGT) 1A1.	trovafloxacin	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-125
27725437-2	2016	Trovafloxacin is mainly metabolized to its acyl-glucuronide by uridine 5"-diphosphate (UDP)-glucuronosyltransferase (UGT) 1A1.	acyl-glucuronide	43-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-125
27725437-2	2016	Trovafloxacin is mainly metabolized to its acyl-glucuronide by uridine 5"-diphosphate (UDP)-glucuronosyltransferase (UGT) 1A1.	Uridine Diphosphate	63-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-125
27725437-4	2016	A UGT1A1-induced cell model was developed and the toxicity of trovafloxacin acyl-glucuronide was evaluated.	trovafloxacin acyl-glucuronide	62-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	2-8
27725437-5	2016	The UGT1A1-induced cell model was developed by treating HepG2 cells with chrysin for 48 h. Chemokine (C-X-C motif) ligand 2, a cytokine involved in drug-induced liver injury, was uniquely induced by trovafloxacin in the UGT1A1-induced HepG2 cells.	trovafloxacin	199-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
27725437-7	2016	An in vivo animal study further demonstrated the importance of UGT1A1 in the trovafloxacin-induced liver toxicity.	trovafloxacin	77-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
26977326-0	2016	Pegvisomant-Induced Cholestatic Hepatitis in an Acromegalic Patient with UGT1A1 (*) 28 Mutation.	pegvisomant	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
25545261-1	2016	BACKGROUND: UGT1A1 is a polymorphic enzyme that has been associated with irinotecan drug metabolisms.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
26512042-9	2016	Axitinib N-glucuronidation was primarily catalyzed by UDP-glucuronosyltransferase (UGT) UGT1A1, which was verified by chemical inhibitors and UGT1A1 null expressers, with lesser contributions from UGTs 1A3, 1A9, and 1A4.	Axitinib	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
26512042-9	2016	Axitinib N-glucuronidation was primarily catalyzed by UDP-glucuronosyltransferase (UGT) UGT1A1, which was verified by chemical inhibitors and UGT1A1 null expressers, with lesser contributions from UGTs 1A3, 1A9, and 1A4.	Axitinib	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
27072236-14	2016	Furthermore, as 5.FU and irinotecan metabolism is complex, numerous genes in addition to DPD and UGT1A1 should be investigated.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
26666247-3	2016	The Gilbert genotype, the UGT1A1*28 allele, is the major known genetic cause of variation in bilirubin.	Bilirubin	93-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
26666247-8	2016	RESULTS: Per UGT1A1*28 allele, odds were increased for any need of supplementary oxygen (odds ratio 1.26; 1.05-1.50) and for BPD (odds ratio 1.71; 1.23-2.39), the need of supplementary oxygen increased by 6.38 days (1.87-10.89), and chance per day of no longer needing supplementary oxygen was reduced (hazard rate 0.84; 0.76-0.93).	Oxygen	81-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
26666247-8	2016	RESULTS: Per UGT1A1*28 allele, odds were increased for any need of supplementary oxygen (odds ratio 1.26; 1.05-1.50) and for BPD (odds ratio 1.71; 1.23-2.39), the need of supplementary oxygen increased by 6.38 days (1.87-10.89), and chance per day of no longer needing supplementary oxygen was reduced (hazard rate 0.84; 0.76-0.93).	Oxygen	185-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
26666247-8	2016	RESULTS: Per UGT1A1*28 allele, odds were increased for any need of supplementary oxygen (odds ratio 1.26; 1.05-1.50) and for BPD (odds ratio 1.71; 1.23-2.39), the need of supplementary oxygen increased by 6.38 days (1.87-10.89), and chance per day of no longer needing supplementary oxygen was reduced (hazard rate 0.84; 0.76-0.93).	Oxygen	185-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
26666247-13	2016	CONCLUSIONS: Compared to the common genotype, UGT1A1*28 genotypes were associated with an increased need of oxygen supplementation and risk of BPD in very preterm newborns.	Oxygen	108-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
26068521-0	2016	Metabolism of the anthelmintic drug niclosamide by cytochrome P450 enzymes and UDP-glucuronosyltransferases: metabolite elucidation and main contributions from CYP1A2 and UGT1A1.	Niclosamide	36-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
26068521-11	2016	Although seven UGT enzymes were able to catalyze glucuronidation of niclosamide, UGT1A1 and 1A3 were the enzymes showed the highest metabolic activities.	Niclosamide	68-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-95
26247833-0	2016	Raloxifene glucuronidation in liver and intestinal microsomes of humans and monkeys: contribution of UGT1A1, UGT1A8 and UGT1A9.	Raloxifene Hydrochloride	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
26134155-13	2016	In vitro phenotyping experiments demonstrated that cabotegravir was metabolized by UDP-glucuronosyltransferase (UGT) 1A1 and UGT1A9.	cabotegravir	51-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-120
26068521-12	2016	Activity correlation analyses demonstrated that UGT1A1 played a predominant role in hepatic glucuronidation of niclosamide, whereas the role of UGT1A3 was negligible.	Niclosamide	111-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
26247833-3	2016	In this study, the in vitro glucuronidation of raloxifene in humans and monkeys was examined using liver and intestinal microsomes and recombinant UGT enzymes (UGT1A1, UGT1A8 and UGT1A9).	Raloxifene Hydrochloride	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
26068521-14	2016	In conclusion, niclosamide was subjected to efficient metabolic reactions hydroxylation and glucuronidation, wherein CYP1A2 and UGT1A1 were the main contributing enzymes, respectively.	Niclosamide	15-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
27803477-5	2016	1) In 2005, information regarding the genetic polymorphism of UGT1A1*28 was described in the package insert of the drug irinotecan in the United States.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
27803477-7	2016	Through clinical research, we demonstrated that UGT1A1*6 was a significant factor for neutropenia, as induced by irinotecan.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
26642944-4	2015	Lapatinib exhibited potent competitive inhibition against UGT1A1 activity with a Ki of 0.5 muM.	Lapatinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
26642944-6	2015	The TKIs also exerted intermediate inhibition against several UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by axitinib; and UGT1A9 by vandetanib).	Imatinib Mesylate	105-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
26642944-7	2015	Results from modeling for the quantitative prediction of DDI risk indicated that the coadministration of lapatinib or imatinib at clinical doses could result in a significant increase in AUC of drugs primarily cleared by UGT1A1 or 2B17.	Lapatinib	105-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	221-227
26642944-7	2015	Results from modeling for the quantitative prediction of DDI risk indicated that the coadministration of lapatinib or imatinib at clinical doses could result in a significant increase in AUC of drugs primarily cleared by UGT1A1 or 2B17.	Imatinib Mesylate	118-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	221-227
26642944-8	2015	Lapatinib and imatinib may cause clinically significant DDIs when co-administered UGT1A1 or 2B17 substrates.	Lapatinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
26642944-8	2015	Lapatinib and imatinib may cause clinically significant DDIs when co-administered UGT1A1 or 2B17 substrates.	Imatinib Mesylate	14-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
26628212-0	2015	Serum bilirubin concentration is modified by UGT1A1 haplotypes and influences risk of type-2 diabetes in the Norfolk Island genetic isolate.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
26628212-5	2015	Strong linkage disequilibrium was observed across a 200 kb region spanning the UDP-glucuronosyltransferase family, including UGT1A1, an enzyme known to metabolise bilirubin.	Bilirubin	163-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
26628212-9	2015	CONCLUSIONS: In summary, a pedigree-based GWAS of blood-based clinical traits in the Norfolk Island population has identified variants within the UDPGT family directly associated with serum bilirubin levels, which is in turn implicated with reduced risk of developing type-2 diabetes within this population.	Bilirubin	190-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-151
25778466-0	2015	A novel UGT1 marker associated with better tolerance against irinotecan-induced severe neutropenia in metastatic colorectal cancer patients.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-12
26664141-0	2015	The relationship between UGT1A1 gene polymorphism and irinotecan effect on extensive-stage small-cell lung cancer.	Irinotecan	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
26664141-11	2015	CONCLUSION: For irinotecan-based regimens in E-SCLC, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for severe adverse events.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
26664141-11	2015	CONCLUSION: For irinotecan-based regimens in E-SCLC, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for severe adverse events.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
26223945-5	2015	RESULTS: One UGT1A1 SNP of rs887829 (C&gt;T) exhibited significant association with stable warfarin doses in the study population and subgroup.	Warfarin	91-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
26223945-10	2015	CONCLUSION: Our results suggest that UGT1A1 could be a determinant of stable warfarin doses.	Warfarin	77-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25216634-2	2015	Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
25216634-2	2015	Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan.	Irinotecan	117-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
25216634-2	2015	Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
26220753-1	2015	Crigler-Najjar syndrome presents as severe unconjugated hyperbilirubinemia and is characteristically caused by a mutation in the UGT1A1 gene, encoding the enzyme responsible for bilirubin glucuronidation.	Bilirubin	61-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
26407805-7	2015	UGT1A1, 1A3, 1A7, 1A8, 1A9, 1A10, 2B4, 2B7 and 2B17 participated in the formation of 4"-O-G, while UGT2B17 demonstrated the highest catalytic activity in this biotransformation.	4"-o-g	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26494856-0	2015	High-Dose FOLFIRI plus Bevacizumab in the Treatment of Metastatic Colorectal Cancer Patients with Two Different UGT1A1 Genotypes: FFCD 0504 Study.	FOLFIRI regimen	10-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
26494856-2	2015	UDP-glucuronosyltransferase: (UGT1A1) polymorphism may be predictive of toxicity and efficacy of irinotecan.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
26494856-3	2015	This phase II study aimed to evaluate the combination of high-dose FOLFIRI plus bevacizumab in patients with previously untreated metastatic colorectal cancer (MCRC) based on their UGT1A1 genotype.	FOLFIRI regimen	67-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-187
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-90
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	160-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-90
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	160-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
26692528-10	2015	CONCLUSIONS: Our study showed that mCRC patients with UGT1A1 *1/*1 and *1/*28 genotypes could receive escalated doses of irinotecan to obtain a more favorable clinical outcome without significant AEs.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
26543529-0	2015	Serum Total Bilirubin, not Cholelithiasis, is Influenced by UGT1A1 Polymorphism, Alpha Thalassemia and beta(s) Haplotype: First Report on Comparison between Arab-Indian and African beta(s) Genes.	Bilirubin	12-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
26348140-3	2015	This study aimed to investigate the inhibitory effects of FP extract and its major constituents against human UDP-glucuronosyltransferase 1A1 (UGT1A1), the key enzyme responsible for metabolic elimination of bilirubin.	Bilirubin	208-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-141
26348140-3	2015	This study aimed to investigate the inhibitory effects of FP extract and its major constituents against human UDP-glucuronosyltransferase 1A1 (UGT1A1), the key enzyme responsible for metabolic elimination of bilirubin.	Bilirubin	208-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
26348140-4	2015	To this end, N-(3-carboxy propyl)-4-hydroxy-1,8-naphthalimide (NCHN), a newly developed specific fluorescent probe for UGT1A1, was used to evaluate the inhibitory effects of FP extract or its fractions in human liver microsomes (HLM), while LC-UV fingerprint and UGT1A1 inhibition profile were combined to identity and characterize the naturally occurring inhibitors of UGT1A1 in FP.	n-(3-carboxy propyl)-4-hydroxy-1,8-naphthalimide	13-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
26692528-0	2015	Clinical Implication of UGT1A1 Promoter Polymorphism for Irinotecan Dose Escalation in Metastatic Colorectal Cancer Patients Treated with Bevacizumab Combined with FOLFIRI in the First-line Setting.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26692528-0	2015	Clinical Implication of UGT1A1 Promoter Polymorphism for Irinotecan Dose Escalation in Metastatic Colorectal Cancer Patients Treated with Bevacizumab Combined with FOLFIRI in the First-line Setting.	FOLFIRI regimen	164-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26692528-1	2015	PURPOSE: This study aimed to identify the efficacy and toxicity of the FOLFIRI regimen (fluorouracil, leucovorin, and irinotecan) with irinotecan dose escalation plus bevacizumab as first-line chemotherapy for metastatic colorectal cancer (mCRC) via UGT1A1 genotyping.	FOLFIRI regimen	71-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	250-256
26692528-1	2015	PURPOSE: This study aimed to identify the efficacy and toxicity of the FOLFIRI regimen (fluorouracil, leucovorin, and irinotecan) with irinotecan dose escalation plus bevacizumab as first-line chemotherapy for metastatic colorectal cancer (mCRC) via UGT1A1 genotyping.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	250-256
26692528-6	2015	RESULTS: The clinical response and disease control rates of mCRC patients treated with FOLFIRI plus bevacizumab were significantly better in patients with UGT1A1 *1/*1 and *1/*28 genotypes than in patients with UGT1A1 *28/*28 (P = .006 and P &lt; .001, respectively).	FOLFIRI regimen	87-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
26692528-6	2015	RESULTS: The clinical response and disease control rates of mCRC patients treated with FOLFIRI plus bevacizumab were significantly better in patients with UGT1A1 *1/*1 and *1/*28 genotypes than in patients with UGT1A1 *28/*28 (P = .006 and P &lt; .001, respectively).	FOLFIRI regimen	87-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	211-217
26342858-3	2015	Bilirubin undergoes selective metabolism by UDP-glucuronosyltransferase (UGT) 1A1 and becomes a water soluble glucuronide.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-81
26429709-7	2015	The study was amended to exclude 4 UGT1A1*28 7/7 homozygous patients due to frequent irinotecan-related grade 3/grade 4 diarrhea and/or febrile neutropenia.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
25649470-0	2015	Interferon and ribavirin combination therapy are linked to severe indirect hyperbilirubinemia in patients with nt-211G &gt; A variant of UGT1A1 gene.	Ribavirin	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
26543529-4	2015	RESULTS: The mean serum total bilirubin level was significantly higher in the homozygous UGT1A1(AT)7 group as compared to UGT1A1(AT)6 group.	Bilirubin	30-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
26543529-5	2015	Thus, not cholelithiasis but total serum bilirubin was influenced by UGT1A1 polymorphism in this SCA cohort.	Bilirubin	41-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
26543529-6	2015	CONCLUSION: As observed in other population groups, the UGT1A1 (AT)7 homozygosity was significantly associated with raised serum total bilirubin level, but the prevalence of gallstones in the Omani SCA patients was not associated with alpha thalassaemia, UGT1A1 polymorphism, or beta(s) haplotypes.	Bilirubin	135-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
26482555-8	2015	UGT1A1 genotyping revealed that patients with UGT1A1 polymorphisms exhibited significantly higher response rates to NAC than those with the wild-type (79.5 vs. 49.5 %, respectively, p &lt; 0.05).	nac	116-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26482555-8	2015	UGT1A1 genotyping revealed that patients with UGT1A1 polymorphisms exhibited significantly higher response rates to NAC than those with the wild-type (79.5 vs. 49.5 %, respectively, p &lt; 0.05).	nac	116-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
26482555-9	2015	CONCLUSIONS: These results indicate that GMP scores of cancerous tissue combined with UGT1A1 genotyping of blood samples may serve as highly potent markers for predicting the efficacy of NAC for individual SCC patients.	nac	187-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
26320626-0	2015	Glucuronidation of bavachinin by human tissues and expressed UGT enzymes: Identification of UGT1A1 and UGT1A8 as the major contributing enzymes.	bavachinin	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
25988789-3	2015	A series of N-substituted derivatives with various hydrophobic, acidic and basic groups were designed and synthesized to evaluate the selectivity of HN derivatives toward UGT1A1.	Nitrogen	12-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
25988789-5	2015	Among the synthesized fluorescent probes, NCHN (N-3-carboxy propyl-4-hydroxy-1,8-naphthalimide) displayed the best combination of selectivity, sensitivity and ratiometric fluorescence response following UGT1A1-catalyzed glucuronidation.	nchn	42-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-209
25988789-5	2015	Among the synthesized fluorescent probes, NCHN (N-3-carboxy propyl-4-hydroxy-1,8-naphthalimide) displayed the best combination of selectivity, sensitivity and ratiometric fluorescence response following UGT1A1-catalyzed glucuronidation.	n-3-carboxy propyl-4-hydroxy-1,8-naphthalimide	48-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-209
25988789-6	2015	UGT1A1-catalyzed NCHN-4-O-glucuronidation generated a single fluorescent product with a high quantum yield (Phi=0.688) and brought remarkable changes in both color and fluorescence in comparison with the parental substrate.	nchn	17-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25988789-6	2015	UGT1A1-catalyzed NCHN-4-O-glucuronidation generated a single fluorescent product with a high quantum yield (Phi=0.688) and brought remarkable changes in both color and fluorescence in comparison with the parental substrate.	4-o	22-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26180128-5	2015	DPF similarly inhibited UGT1A1, UGT1A9, and UGT1A10, with IC50 values ranging from 39 to 66 microM.	dapagliflozin	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26180128-8	2015	Consistent with the activity screening data, DPF was a less potent inhibitor of UGT1A1 and UGT1A9.	dapagliflozin	45-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
26180128-9	2015	The Ki for DPF inhibition of UGT1A1 was 81 microM, whereas the Ki values for inhibition of UGT1A9 ranged from 12 to 15 microM.	dapagliflozin	11-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
26320626-4	2015	Reaction phenotyping assay showed that UGT1A1, UGT1A3 and UGT1A8 were involved in BCI-4"-O-glucuronidation, while UGT1A1 and UGT1A8 displayed the higher catalytic ability among all tested UGT isoforms.	bci-4"-o	82-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
26320626-4	2015	Reaction phenotyping assay showed that UGT1A1, UGT1A3 and UGT1A8 were involved in BCI-4"-O-glucuronidation, while UGT1A1 and UGT1A8 displayed the higher catalytic ability among all tested UGT isoforms.	bci-4"-o	82-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
26320626-5	2015	Kinetic analysis demonstrated that BCI-4"-O-glucuronidation in both HLM and UGT1A1 followed sigmoidal kinetic behaviors and displayed much close Km values (12.4 muM in HLM &amp; 9.7 muM in UGT1A1).	bci-4"-o	35-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
26320626-5	2015	Kinetic analysis demonstrated that BCI-4"-O-glucuronidation in both HLM and UGT1A1 followed sigmoidal kinetic behaviors and displayed much close Km values (12.4 muM in HLM &amp; 9.7 muM in UGT1A1).	bci-4"-o	35-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
26320626-5	2015	Kinetic analysis demonstrated that BCI-4"-O-glucuronidation in both HLM and UGT1A1 followed sigmoidal kinetic behaviors and displayed much close Km values (12.4 muM in HLM &amp; 9.7 muM in UGT1A1).	Adenosine Monophosphate	173-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
26320626-6	2015	Both chemical inhibition assays and correlation analysis demonstrated that UGT1A1 displayed a predominant role in BCI-4"-O-glucuronidation in HLM.	bci-4"-o	114-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
26320626-9	2015	These findings suggested that UGT1A1 and UGT1A8 were the primary isoforms involved in BCI-4"-O-glucuronidation in HLM, and HIM, respectively.	bci-4"-o	86-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
26233886-0	2015	Correlation between UGT1A1 polymorphisms and raltegravir plasma trough concentrations in Japanese HIV-1-infected patients.	Raltegravir Potassium	45-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
26233886-1	2015	Raltegravir (RAL), an HIV integrase inhibitor, is metabolized mainly by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-103
26233886-1	2015	Raltegravir (RAL), an HIV integrase inhibitor, is metabolized mainly by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
26210671-9	2015	Therefore, nicotine-treated hUGT1 mice might be useful to investigate the role of brain UGT1A3 in the regulation of local levels of these drugs and their response.	Nicotine	11-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-33
26163112-8	2015	Glucuronidation of homoegonol to M5 was mediated by UGT1A1, UGT1A3, UGT1A4, and UGT2B7 enzymes, whereas M4 was formed from 4-O-demethylhomoegonol by UGT1A1, UGT1A8, UGT1A10, and UGT2B15 enzymes.	homoegonol	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
26163112-8	2015	Glucuronidation of homoegonol to M5 was mediated by UGT1A1, UGT1A3, UGT1A4, and UGT2B7 enzymes, whereas M4 was formed from 4-O-demethylhomoegonol by UGT1A1, UGT1A8, UGT1A10, and UGT2B15 enzymes.	homoegonol	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
26413716-15	2015	In addition, our findings indicate that similar to the adult population, the UGT1A1 is the main locus responsible for normal variation of serum bilirubin in pediatric populations.	Bilirubin	144-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
25782327-0	2015	DPD and UGT1A1 deficiency in colorectal cancer patients receiving triplet chemotherapy with fluoropyrimidines, oxaliplatin and irinotecan.	fluoropyrimidines	92-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
25782327-0	2015	DPD and UGT1A1 deficiency in colorectal cancer patients receiving triplet chemotherapy with fluoropyrimidines, oxaliplatin and irinotecan.	Oxaliplatin	111-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
25782327-0	2015	DPD and UGT1A1 deficiency in colorectal cancer patients receiving triplet chemotherapy with fluoropyrimidines, oxaliplatin and irinotecan.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
25782327-2	2015	Single nucleotide polymorphisms (SNPs) in DPYD and UGT1A1 influence fluoropyrimdines and irinotecan adverse events (AEs).	fluoropyrimdines	68-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
25782327-2	2015	Single nucleotide polymorphisms (SNPs) in DPYD and UGT1A1 influence fluoropyrimdines and irinotecan adverse events (AEs).	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
26072390-8	2015	Poor responders had a higher conjugated/unconjugated bilirubin ratio, indicating increased UGT1A1 activity.	Bilirubin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
26247603-10	2015	There are human-specific changes in the sequence of the promoter and the protein-coding sequence of uridine diphosphoglucuronosyltransferase 1 (UGT1A1), the enzyme that transforms bilirubin and toxic plant compounds into water-soluble, excretable metabolites.	Bilirubin	180-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
26247603-10	2015	There are human-specific changes in the sequence of the promoter and the protein-coding sequence of uridine diphosphoglucuronosyltransferase 1 (UGT1A1), the enzyme that transforms bilirubin and toxic plant compounds into water-soluble, excretable metabolites.	Water	221-226	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
26247603-11	2015	Experimental evidence that UGT1A1 is down-regulated in the human liver suggests that changes in the promoter may be responsible for the human-specific increase in bilirubin.	Bilirubin	163-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
26247603-12	2015	We speculate that since cooking reduces toxic plant compounds, consumption of cooked foods, which is specific to humans, may have resulted in relaxed constraint on UGT1A1 which has in turn led to higher serum levels of bilirubin in humans.	Bilirubin	219-228	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
25611851-9	2015	Furthermore, we reported our present work on genetic analysis of mutations of UGT1A1 gene, and the correlation of UGT1A1 mutations with serum total bilirubin levels in Taiwanese population.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
26229432-0	2015	Relationship between UGT1A1*6/*28 polymorphisms and severe toxicities in Chinese patients with pancreatic or biliary tract cancer treated with irinotecan-containing regimens.	Irinotecan	143-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
26229432-1	2015	PURPOSE: The aim of this retrospective study was to investigate the relationship between UGT1A1 polymorphisms and toxicities in Chinese patients with pancreatic or biliary tract cancer receiving irinotecan-containing regimens as the second- or third-line chemotherapy.	Irinotecan	195-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
26229432-12	2015	CONCLUSION: In Chinese patients with pancreatic or biliary tract cancer administered irinotecan-containing regimens, those with UGT1A1*6 variant may have a high risk of severe neutropenia.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
26146841-3	2015	Eleven common mutations and polymorphisms across five bilirubin metabolism genes, namely those encoding UGT1A1, HMOX1, BLVRA, SLCO1B1 and SLCO1B3, were determined using the high resolution melt (HRM) assay or PCR-capillary electrophoresis analysis.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
26066637-0	2015	Decreased Expression of Multidrug Resistance-Associated Protein 4 (MRP4/ABCC4) Leads to Reduced Glucuronidation of Flavonoids in UGT1A1-Overexpressing HeLa Cells: The Role of Futile Recycling.	Flavonoids	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
25870101-0	2015	Glucuronidation of OTS167 in Humans Is Catalyzed by UDP-Glucuronosyltransferases UGT1A1, UGT1A3, UGT1A8, and UGT1A10.	OTS167	19-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
25870101-6	2015	Nilotinib (UGT1A1 inhibitor) and emodin (UGT1A8 and UGT1A10 inhibitor) exhibited the highest inhibitory effects on OTS167-G formation in HLM (68%) and HIM (47%).	nilotinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
26180834-0	2015	Screening for UGT1A1 Genotype in Study A5257 Would Have Markedly Reduced Premature Discontinuation of Atazanavir for Hyperbilirubinemia.	Atazanavir Sulfate	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
26180834-3	2015	Atazanavir-associated hyperbilirubinemia correlates with UGT1A1 rs887829 genotype.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
26180834-6	2015	Discriminatory properties of UGT1A1 T/T genotype for predicting bilirubin-related atazanavir discontinuation through 96 weeks after antiretroviral initiation were estimated.	Bilirubin	64-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
26180834-6	2015	Discriminatory properties of UGT1A1 T/T genotype for predicting bilirubin-related atazanavir discontinuation through 96 weeks after antiretroviral initiation were estimated.	Atazanavir Sulfate	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
26591441-0	2015	[UGT1A1 Genotyping for Proper Use of Irinotecan].	Irinotecan	37-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	1-7
26591441-3	2015	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by the UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-135
26591441-3	2015	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by the UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	41-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-135
26591441-4	2015	Recent pharmacogenetic studies on irinotecan have revealed the impact of UGT1A1 polymorphisms on severe adverse effects.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
26591441-5	2015	A variant in the promoter of the UGT1A1 gene, the UGT1A1 *28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and severe toxicities of irinotecan have been reported.	Irinotecan	178-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26591441-5	2015	A variant in the promoter of the UGT1A1 gene, the UGT1A1 *28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and severe toxicities of irinotecan have been reported.	Irinotecan	178-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26591441-9	2015	For patients showing homozygosity for UGT1A1*28, *6, or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
26591441-9	2015	For patients showing homozygosity for UGT1A1*28, *6, or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
26591441-11	2015	Moreover, a recent Phase 2 trial for FOLFIRINOX in Japan excluded patients who showed homozygosity for UGT1A1*28, *6, or compound heterozygosity for UGT1A1*6 and *28.	folfirinox	37-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
26591441-11	2015	Moreover, a recent Phase 2 trial for FOLFIRINOX in Japan excluded patients who showed homozygosity for UGT1A1*28, *6, or compound heterozygosity for UGT1A1*6 and *28.	folfirinox	37-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
26591441-12	2015	At present, irinotecan chemotherapy based on a patient"s UGT1A1 genetic status is scientifically reasonable.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
25834030-7	2015	We found that zafirlukast is a potent general inhibitor of UGT1As and a moderate inhibitor of UGT2Bs because it monitors 4-methylumbelliferone glucuronidation by recombinant UGTs.	zafirlukast	14-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-63
26125934-0	2015	Correlation of UGT1A1 and ERCC1 gene polymorphisms with the outcome of combined irinotecan plus cisplatin treatment in recurrent ovarian cancer.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26125934-0	2015	Correlation of UGT1A1 and ERCC1 gene polymorphisms with the outcome of combined irinotecan plus cisplatin treatment in recurrent ovarian cancer.	Cisplatin	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26125934-1	2015	The aim of this study was to define the genotypes of UGT1A1 and ERCC1 and to examine their relationship with the efficacy and toxicity of a combination therapy of irinotecan and cisplatin in patients with advanced ovarian cancer.	Irinotecan	163-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
26125934-1	2015	The aim of this study was to define the genotypes of UGT1A1 and ERCC1 and to examine their relationship with the efficacy and toxicity of a combination therapy of irinotecan and cisplatin in patients with advanced ovarian cancer.	Cisplatin	178-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
26125934-7	2015	Together, the results from this study suggest that UGT1A1 is a target gene for tardive diarrhea, and that the UGT1A1*28 gene mutation might increase the risk of diarrhea with irinotecan-based chemotherapy.	Irinotecan	175-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
26125934-7	2015	Together, the results from this study suggest that UGT1A1 is a target gene for tardive diarrhea, and that the UGT1A1*28 gene mutation might increase the risk of diarrhea with irinotecan-based chemotherapy.	Irinotecan	175-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
25917289-4	2015	Our data indicated that both gefitinib and DMG are potent inhibitors of SN-38 glucuronidation via UGT1A1 inhibition.	Gefitinib	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
25917289-4	2015	Our data indicated that both gefitinib and DMG are potent inhibitors of SN-38 glucuronidation via UGT1A1 inhibition.	dimethylglycine	43-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
25917289-4	2015	Our data indicated that both gefitinib and DMG are potent inhibitors of SN-38 glucuronidation via UGT1A1 inhibition.	Irinotecan	72-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
25315738-6	2015	Uridine diphospho-glucuronosyl transferase 1A1 (UGT1A1) is responsible for the glucuronidation of bilirubin; deficiency of this enzyme results in unconjugated hyperbilirubinaemia.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-46
25315738-6	2015	Uridine diphospho-glucuronosyl transferase 1A1 (UGT1A1) is responsible for the glucuronidation of bilirubin; deficiency of this enzyme results in unconjugated hyperbilirubinaemia.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
25817555-4	2015	The present review on the impact of the deficient UGT1A1*28 variant on irinotecan efficacy and toxicity was produced by a French joint workgroup comprising the Group of Clinical Onco-pharmacology (GPCO-Unicancer) and the National Pharmacogenetics Network (RNPGx).	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25817555-5	2015	It clearly emerges that for irinotecan doses at least equal to 180 mg/m(2) , patients homozygous for the UGT1A1*28 allele are at increased risk of developing hematological and/or digestive toxicities.	Irinotecan	28-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
25081908-11	2015	A significant inverse correlation (P = 0.03) was observed between CDFX and UGT1A1*28 gene polymorphism, but only in patients with levels of lean body mass (LBM) below the median (P for interaction = 0.05).	cdfx	66-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
26039129-11	2015	UGT1A1 intronic single-nucleotide polymorphisms (SNPs) (rs6742078, rs887829, rs4148324) serve as proxy markers for the low-frequency and rare UGT1A1 variants, thereby providing mechanistic explanation to the relationship between UGT1A1 intronic SNPs and the UGT1A1 enzyme activity.	single-nucleotide	16-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26039129-11	2015	UGT1A1 intronic single-nucleotide polymorphisms (SNPs) (rs6742078, rs887829, rs4148324) serve as proxy markers for the low-frequency and rare UGT1A1 variants, thereby providing mechanistic explanation to the relationship between UGT1A1 intronic SNPs and the UGT1A1 enzyme activity.	single-nucleotide	16-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
26039129-11	2015	UGT1A1 intronic single-nucleotide polymorphisms (SNPs) (rs6742078, rs887829, rs4148324) serve as proxy markers for the low-frequency and rare UGT1A1 variants, thereby providing mechanistic explanation to the relationship between UGT1A1 intronic SNPs and the UGT1A1 enzyme activity.	single-nucleotide	16-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
26039129-11	2015	UGT1A1 intronic single-nucleotide polymorphisms (SNPs) (rs6742078, rs887829, rs4148324) serve as proxy markers for the low-frequency and rare UGT1A1 variants, thereby providing mechanistic explanation to the relationship between UGT1A1 intronic SNPs and the UGT1A1 enzyme activity.	single-nucleotide	16-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
25993113-3	2015	In East Asian populations, the compound homozygous UGT1A1 G71R and Y486D variants are frequently observed in cases with bilirubin levels exceeding 200 mumol/L.	Bilirubin	120-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
25993113-8	2015	Therefore, we propose that the spectrum of UGT1A1 variations in CNS-II differs according to the bilirubin levels.	Bilirubin	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	200-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	232-242	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25880011-2	2015	We prospectively studied the relation between the UGT1A1 genotype and the safety of irinotecan-based regimens in Japanese patients with advanced colorectal cancer, and then constructed a nomogram for predicting the risk of severe neutropenia in the first treatment cycle.	Irinotecan	84-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25880011-6	2015	RESULTS: The UGT1A1 genotype was confirmed to be associated with increased risks of irinotecan-induced grade 3 or 4 neutropenia and diarrhoea.	Irinotecan	84-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25966095-1	2015	Mutations in the UGT1A1 gene cause Crigler-Najjar syndrome (CN), which causes non-hemolytic unconjugated hyperbilirubinemia, and is categorized as CN1 and CN2 according to the severity of bilirubin levels.	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
25595598-0	2015	Characterization of chrysin glucuronidation in UGT1A1-overexpressing HeLa cells: elucidating the transporters responsible for efflux of glucuronide.	Glucuronides	136-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
25595598-5	2015	Ko143 at 10-20 muM (a dual inhibitor of BCRP and UGT1A1) caused a marked decrease (51.3%-59.7%, P &lt; 0.01) in the excretion rate and efflux clearance of CG.	3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl ester	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
25595598-5	2015	Ko143 at 10-20 muM (a dual inhibitor of BCRP and UGT1A1) caused a marked decrease (51.3%-59.7%, P &lt; 0.01) in the excretion rate and efflux clearance of CG.	cg	155-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
25595598-6	2015	Likewise, MK-571 at 5-20 muM (an inhibitor of MRPs but an activator of UGT1A1) resulted in a significant reduction in the excretion rate (18.2%-64.0%, P &lt; 0.01) and efflux clearance (37.0%-90.2%, P &lt; 0.001).	verlukast	10-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
26039129-6	2015	These variants were in strong linkage disequilibrium with 3 intronic UGT1A1 variants (rs887829, rs4148325, rs6742078), which were significantly associated with total bilirubin level (P = 2.34 x 10(-34), P = 7.02 x 10(-34), and P = 8.27 x 10(-34)), as well as unconjugated, and conjugated bilirubin levels.	Bilirubin	166-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
26039129-6	2015	These variants were in strong linkage disequilibrium with 3 intronic UGT1A1 variants (rs887829, rs4148325, rs6742078), which were significantly associated with total bilirubin level (P = 2.34 x 10(-34), P = 7.02 x 10(-34), and P = 8.27 x 10(-34)), as well as unconjugated, and conjugated bilirubin levels.	Bilirubin	288-297	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
26039129-10	2015	Using an exome-wide approach we identified coding variants on UGT1A1 and UGT1A6 genes in association with serum bilirubin level and hyperbilirubinemia risk in elderly subjects.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25348619-2	2015	Our aim was to evaluate DFX plasma concentrations according to single-nucleotide polymorphisms in genes involved in its metabolism (UGT1A1, UGT1A3, CYP1A1, CYP1A2 and CYP2D6) and elimination (MRP2 and BCRP1).	Deferasirox	24-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
25522350-6	2015	Diflunisal inhibited the UGT1A1 (IC50 = 33.0 mum) and UGT1A9 (IC50 = 19.4 mum).	Diflunisal	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
25981652-2	2015	However, there are reports of an association between certain UGT1A1 genetic polymorphisms and the development of adverse reactions(such as neutropenia)related to irinotecan metabolism.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25981652-7	2015	These results suggest that a dose reduction of irinotecan should be considered for patients who fall into the homozygous group upon analysis of their UGT1A1 genetic polymorphisms, as such patients might be susceptible to grade 4 neutropenia.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
25081908-14	2015	Interesting results emerged from the analysis of genetic and physical characteristics of patients: LBM was a borderline significant effect modifier of the relationship between UGT1A1 polymorphisms and CDFX .	cdfx	201-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
25663682-7	2015	Haploinsufficiency at MLXIPL and increased penetrance for hypomorphic alleles at the UGT1A1 gene promoter might underlie the lipid and bilirubin alterations.	Bilirubin	135-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
25171434-0	2015	UGT1A1*28 is associated with greater decrease in serum K+ levels following oral intake of procaterol.	Procaterol	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25171434-8	2015	Meanwhile, overall serum K(+) level changes were significantly lower in carriers of UGT1A1*28 than in non-carriers after correcting for strong effects of serum procaterol concentrations and baseline K(+) levels.	Procaterol	160-170	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
25171434-11	2015	CONCLUSION: The present study indicates that significant hypokalemia may occur in carriers of UGT1A1*28 by systemic administration of procaterol and potentially by other beta2-agonists metabolized in the liver.	Procaterol	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25834402-16	2015	CONCLUSION: In mCRC patients with wild-type or heterozygous UGT1A1*6 or *28 genotype, biweekly XELIRI + BV is effective and feasible as second-line chemotherapy.	xeliri + bv	95-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
26375741-5	2015	The relationship between A(TA)nTAA variation of UGT1A1 gene, the serum bilirubin level and the occurrence of cholilithiasis was investigated.	Bilirubin	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
26375741-5	2015	The relationship between A(TA)nTAA variation of UGT1A1 gene, the serum bilirubin level and the occurrence of cholilithiasis was investigated.	cholilithiasis	109-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
24905729-11	2015	In vitro, rifampicin PXR-dependently upregulated biotransformation phase 1 (CYP3A4), phase 2 (UGT1A1) and phase 3 (MRP2) enzymes/carriers as well as the basolateral bile salt exporter OSTbeta.	Rifampin	10-20	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
24905729-14	2015	PXR-dependent induction of CYP3A4, UGT1A1, MRP2 and OSTbeta could contribute to the anticholestatic effect of rifampicin in PHSF.	Rifampin	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
26012253-5	2015	Inhibition kinetic type and parameter (Ki) were determined for the inhi- bition of podophyllotoxin towards UGT1A1, and competitive inhibition of podophyllotoxin towards UGT1A1 was observed with the inhibition kinetic parameter (Ki) to be 4.0 muM.	Podophyllotoxin	83-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
26012253-5	2015	Inhibition kinetic type and parameter (Ki) were determined for the inhi- bition of podophyllotoxin towards UGT1A1, and competitive inhibition of podophyllotoxin towards UGT1A1 was observed with the inhibition kinetic parameter (Ki) to be 4.0 muM.	Podophyllotoxin	145-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
26012253-7	2015	In conclusion, podophyllotoxin inhibited UGT1A1 activity, indicating potential herb-drug interactions between podophyllotoxin-containing herbs and drugs mainly undergoing UGT1A1-mediated metabolism.	Podophyllotoxin	15-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
26012253-7	2015	In conclusion, podophyllotoxin inhibited UGT1A1 activity, indicating potential herb-drug interactions between podophyllotoxin-containing herbs and drugs mainly undergoing UGT1A1-mediated metabolism.	Podophyllotoxin	15-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
26012253-7	2015	In conclusion, podophyllotoxin inhibited UGT1A1 activity, indicating potential herb-drug interactions between podophyllotoxin-containing herbs and drugs mainly undergoing UGT1A1-mediated metabolism.	Podophyllotoxin	110-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
26012253-7	2015	In conclusion, podophyllotoxin inhibited UGT1A1 activity, indicating potential herb-drug interactions between podophyllotoxin-containing herbs and drugs mainly undergoing UGT1A1-mediated metabolism.	Podophyllotoxin	110-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
25596428-2	2015	DES can potently inhibit E2-3-O-glucuronidation in HLM, a probe reaction for UGT1A1.	Diethylstilbestrol	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
25611302-2	2015	The active metabolite of irinotecan, SN-38, is a known substrate of drug-metabolising enzymes, including UGT1A1, as well as OATP and ABC drug transporters.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
25576848-2	2015	Gilbert"s Syndrome is associated with mutation in the Uridine Glucuronosyl Transferase 1A1 (UGT1A1) gene promoter, reducing UGT1A1 activity, which normally conjugates bilirubin allowing its elimination from the blood.	Bilirubin	167-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-90
25576848-2	2015	Gilbert"s Syndrome is associated with mutation in the Uridine Glucuronosyl Transferase 1A1 (UGT1A1) gene promoter, reducing UGT1A1 activity, which normally conjugates bilirubin allowing its elimination from the blood.	Bilirubin	167-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
25576848-2	2015	Gilbert"s Syndrome is associated with mutation in the Uridine Glucuronosyl Transferase 1A1 (UGT1A1) gene promoter, reducing UGT1A1 activity, which normally conjugates bilirubin allowing its elimination from the blood.	Bilirubin	167-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
25858605-4	2015	Dolutegravir is metabolized by UGT1A1 and, to a lesser extent, by CYP3A4, without being an inducer or inhibitor of the usual metabolic systems.	dolutegravir	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
25611302-2	2015	The active metabolite of irinotecan, SN-38, is a known substrate of drug-metabolising enzymes, including UGT1A1, as well as OATP and ABC drug transporters.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
25611302-5	2015	RESULTS: SLCO1B1 521C was significantly associated with increased SN-38 exposure (P&lt;0.001), which was additive with UGT1A1*28.	Irinotecan	66-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
25596428-10	2015	In summary, this study issues new potential toxic mechanisms for DES: potently inhibiting the activity of UGT1A1 and powerfully accelerating the formation of cholestatic E2-17-O-glucuronide by UGT1A4.	Diethylstilbestrol	65-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
25052959-4	2015	HS-23 showed negligible inhibition of CYP1A2, CYP2C8, CYP2D6, UGT1A1, UGT1A4, UGT1A9, and UGT2B7 activities in human liver microsomes.	hs-23	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25692465-0	2015	UDP-glucuronosyltransferase 1A determinates intracellular accumulation and anti-cancer effect of beta-lapachone in human colon cancer cells.	beta-lapachone	97-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	7-ethyl-10-hydroxycamptothecin glucuronide	150-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	7-ethyl-10-hydroxycamptothecin glucuronide	150-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25760534-0	2015	UDP-glucuronosyltransferase (UGT) 1A1 mainly contributes to the glucuronidation of trovafloxacin.	trovafloxacin	83-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
25760534-5	2015	In human liver microsomes, trovafloxacin acyl-glucuronidation followed the Hill equation with S50 value of 95 muM, Vmax value of 243 pmol/min per mg, and a Hill coefficient of 2.0, while the UGT1A1-expressing system displayed Michaelis-Menten kinetics with a substrate inhibition, with Km value of 759 muM and Vmax value of 1160 pmol/min per mg.	trovafloxacin	27-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
25760534-6	2015	In human liver microsomes prepared from poor metabolizers (UGT1A1*28/*28), significantly reduced trovafloxacin acyl-glucuronide formation activity was observed, indicating that UGT1A1 mainly, while other UGT members such as UGT1A3 and UGT1A9 partially, contributes to the glucuronidation of trovafloxacin.	trovafloxacin	97-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
25760534-6	2015	In human liver microsomes prepared from poor metabolizers (UGT1A1*28/*28), significantly reduced trovafloxacin acyl-glucuronide formation activity was observed, indicating that UGT1A1 mainly, while other UGT members such as UGT1A3 and UGT1A9 partially, contributes to the glucuronidation of trovafloxacin.	trovafloxacin	97-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
25760534-3	2015	In the present study, among the functional human UGT members, UGT1A1, UGT1A3, and UGT1A9 exhibited higher trovafloxacin acyl-glucuronidation activities.	trovafloxacin	106-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25760534-6	2015	In human liver microsomes prepared from poor metabolizers (UGT1A1*28/*28), significantly reduced trovafloxacin acyl-glucuronide formation activity was observed, indicating that UGT1A1 mainly, while other UGT members such as UGT1A3 and UGT1A9 partially, contributes to the glucuronidation of trovafloxacin.	acyl-glucuronide	111-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
25760534-6	2015	In human liver microsomes prepared from poor metabolizers (UGT1A1*28/*28), significantly reduced trovafloxacin acyl-glucuronide formation activity was observed, indicating that UGT1A1 mainly, while other UGT members such as UGT1A3 and UGT1A9 partially, contributes to the glucuronidation of trovafloxacin.	acyl-glucuronide	111-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
25997248-0	2015	UGT1A1*28 polymorphism influences glucuronidation of bazedoxifene.	bazedoxifene	53-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25760534-6	2015	In human liver microsomes prepared from poor metabolizers (UGT1A1*28/*28), significantly reduced trovafloxacin acyl-glucuronide formation activity was observed, indicating that UGT1A1 mainly, while other UGT members such as UGT1A3 and UGT1A9 partially, contributes to the glucuronidation of trovafloxacin.	trovafloxacin	291-304	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
25760534-6	2015	In human liver microsomes prepared from poor metabolizers (UGT1A1*28/*28), significantly reduced trovafloxacin acyl-glucuronide formation activity was observed, indicating that UGT1A1 mainly, while other UGT members such as UGT1A3 and UGT1A9 partially, contributes to the glucuronidation of trovafloxacin.	trovafloxacin	291-304	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
25997248-3	2015	It has already been shown that a relatively common UGT1A1*28 polymorphism can considerably affect raloxifene pharmacokinetics and pharmacodynamics.	Raloxifene Hydrochloride	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
25997248-4	2015	As pharmacokinetics of bazedoxifene and raloxifene are very similar, the influence of UGT1A1*28 polymorphism on metabolism of bazedoxifene was investigated by genotyped microsomes.	bazedoxifene	126-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
25997248-5	2015	Our results indicate an influence of UGT1A1*28 allele on the formation clearance of both bazedoxifene metabolites.	bazedoxifene	89-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25997248-7	2015	In conclusion, the significant UGT1A1*28 genotype effect on bazedoxifene intrinsic metabolic clearance indicates that this subject is worth further exploration in vivo and provides valuable information research in this field.	bazedoxifene	60-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
25055799-0	2015	UGT1A1 *6 polymorphism predicts outcome in elderly patients with relapsed or refractory diffuse large B-cell lymphoma treated with carboplatin, dexamethasone, etoposide and irinotecan.	Carboplatin	131-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25598834-2	2015	RAL should be double-dosed to 800 mg semi-daily in situation of rifampicin co-medication, because RAL is more rapidly metabolized due to rifampicin-induced Uridine-5"-diphosph- gluronosyl-transferase (UGT1A1).	Rifampin	137-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
25055799-3	2015	The 2-year survival rate after initial CDE-11 treatment was significantly higher in patients with than without UGT1A1*6 (57% vs. 5%).	cde-11	39-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
25055799-0	2015	UGT1A1 *6 polymorphism predicts outcome in elderly patients with relapsed or refractory diffuse large B-cell lymphoma treated with carboplatin, dexamethasone, etoposide and irinotecan.	Dexamethasone	144-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25055799-7	2015	The response to CDE-11 likely correlated with UGT1A1*6 polymorphisms, but further prospective studies are warranted to optimize irinotecan-based chemotherapies relative to UGT1A1 polymorphism.	cde-11	16-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
25055799-0	2015	UGT1A1 *6 polymorphism predicts outcome in elderly patients with relapsed or refractory diffuse large B-cell lymphoma treated with carboplatin, dexamethasone, etoposide and irinotecan.	Etoposide	159-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25055799-0	2015	UGT1A1 *6 polymorphism predicts outcome in elderly patients with relapsed or refractory diffuse large B-cell lymphoma treated with carboplatin, dexamethasone, etoposide and irinotecan.	Irinotecan	173-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25845873-3	2015	From the interaction between atazanavir and DTG via CYP3A4 and UGT1A1 and placental efflux transporter inhibition and considering the infant"s probable enzymatic immaturity, the DTG elimination half-life was estimated to be 4-fold longer in neonates than in adults.	Atazanavir Sulfate	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
25385099-2	2015	Faldaprevir is known to inhibit P-glycoprotein, CYP3A4, and UDP-glucuronosyltransferase 1A1.	faldaprevir	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-91
25845873-3	2015	From the interaction between atazanavir and DTG via CYP3A4 and UGT1A1 and placental efflux transporter inhibition and considering the infant"s probable enzymatic immaturity, the DTG elimination half-life was estimated to be 4-fold longer in neonates than in adults.	dolutegravir	44-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
25808438-5	2015	For upfront identification of patients at high risk of suffering from severe therapy-related toxicity, specific variants of dihydropyrimidine dehydrogenase may be measured for predicting toxicity from fluoropyrimidines and uridine diphosphate glucuronosyltransferase*28 (UGT1A1*28) for predicting toxicity from irinotecan.	fluoropyrimidines	201-218	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
26632182-2	2015	UGT1A1 enzyme activity is commonly evaluated by detecting the elimination of bilirubin substrate or the generation of bilirubin glucuronides.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26632182-2	2015	UGT1A1 enzyme activity is commonly evaluated by detecting the elimination of bilirubin substrate or the generation of bilirubin glucuronides.	Bilirubin	118-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
26632182-2	2015	UGT1A1 enzyme activity is commonly evaluated by detecting the elimination of bilirubin substrate or the generation of bilirubin glucuronides.	Glucuronides	128-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25947908-6	2015	For patients with a UGT1A1*6/*6, *6/*28, or *28/*28 genotype initially administered 300-400 mg/d, a target nilotinib C0 of 500 ng/mL is recommended to prevent elevation of bilirubin levels, whereas for patients with the UGT1A1*1 allele initially administered 600 mg/d, a target nilotinib C0 of 800 ng/mL is recommended.	nilotinib c0	107-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
26087609-0	2015	[The role of assessing UGT1A1 gene polymorphism in the prediction of irinotecan-induced toxicity in the course of chemotherapy for colorectal cancer].	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
25427841-0	2015	A phase I study of UGT1A1 *28/*6 genotype-directed dosing of irinotecan (CPT-11) in Korean patients with metastatic colorectal cancer receiving FOLFIRI.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
25427841-0	2015	A phase I study of UGT1A1 *28/*6 genotype-directed dosing of irinotecan (CPT-11) in Korean patients with metastatic colorectal cancer receiving FOLFIRI.	Irinotecan	73-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
25427841-0	2015	A phase I study of UGT1A1 *28/*6 genotype-directed dosing of irinotecan (CPT-11) in Korean patients with metastatic colorectal cancer receiving FOLFIRI.	FOLFIRI regimen	144-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
25427841-1	2015	PURPOSE: A UGT1A1 genotype-directed dose escalation of irinotecan (CPT-11) was performed in patients with metastatic colorectal cancer receiving first-line FOLFIRI chemotherapy.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
25427841-1	2015	PURPOSE: A UGT1A1 genotype-directed dose escalation of irinotecan (CPT-11) was performed in patients with metastatic colorectal cancer receiving first-line FOLFIRI chemotherapy.	Irinotecan	67-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
25427841-8	2015	CONCLUSIONS: The MTD of irinotecan differed according to the UGT1A1 genotype, and higher doses of irinotecan are feasible with sLV5FU2 compared to the present regulatory approved doses.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25427841-8	2015	CONCLUSIONS: The MTD of irinotecan differed according to the UGT1A1 genotype, and higher doses of irinotecan are feasible with sLV5FU2 compared to the present regulatory approved doses.	Irinotecan	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25714435-7	2015	Enzyme kinetic studies showed that UGT1A1 was the main UGT isoform involved in OCG in HLMs.	CHEMBL1234931	79-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
25475995-10	2015	Characterization of UGT isoenzymes in glucuronidation of tanzisertib and CC-418424 revealed that, tanzisertib glucuronide was catalyzed by: UGT1A1, 1A4, 1A10 and 2B4, while CC-418424 glucuronidation was catalyzed by UGT2B4 and 2B7.	4-(9-(tetrahydrofuran-3-yl)-8-(2,4,6-trifluorophenylamino)-9H-purin-2-ylamino)cyclohexanol	57-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
25475995-10	2015	Characterization of UGT isoenzymes in glucuronidation of tanzisertib and CC-418424 revealed that, tanzisertib glucuronide was catalyzed by: UGT1A1, 1A4, 1A10 and 2B4, while CC-418424 glucuronidation was catalyzed by UGT2B4 and 2B7.	cc-418424	73-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
25475995-10	2015	Characterization of UGT isoenzymes in glucuronidation of tanzisertib and CC-418424 revealed that, tanzisertib glucuronide was catalyzed by: UGT1A1, 1A4, 1A10 and 2B4, while CC-418424 glucuronidation was catalyzed by UGT2B4 and 2B7.	tanzisertib glucuronide	98-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
25751380-5	2015	RESULTS: Sequencing of the Gilbert syndrome-associated gene, UGT 1A 1, revealed mutations in the upstream promoter phenobarbital-responsive element module (PBREM) (-3279 mutation, 23 cases), in the promoter TATA box (a TA insertion mutation, 21 cases), and in the coding region of exon 1 (a GGA-AGA Gly71Arg mutation, 18 cases); there was no statistical difference found for any of the three mutations among this patient population (x2 =1.640, P more than 0.05).	Phenobarbital	115-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-69
26068529-2	2015	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an irreplaceable role in detoxification of bilirubin and many drugs (e.g., SN-38).	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
26068529-2	2015	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an irreplaceable role in detoxification of bilirubin and many drugs (e.g., SN-38).	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26068529-2	2015	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an irreplaceable role in detoxification of bilirubin and many drugs (e.g., SN-38).	Irinotecan	122-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
26068529-2	2015	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an irreplaceable role in detoxification of bilirubin and many drugs (e.g., SN-38).	Irinotecan	122-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
25151207-3	2014	METHODS: Nineteen SNPs in the ABCB1, NR1I2, UGT1A1, SLCO1B1 and CYP3A5 genes were examined in case patients with atazanavir/ritonavir-induced nephrolithiasis (n = 31) and controls (n = 47).	Atazanavir Sulfate	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
26068529-5	2015	Determination of glucuronidation rates (beta-estradiol and SN-38 as the substrates) was performed using HeLa1A1 cells and uridine diphosphoglucuronic acid (UDPGA)-supplemented cDNA expressed UGT1A1 enzyme (or microsomes).	Uridine Diphosphate Glucuronic Acid	122-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
25202035-1	2014	OBJECTIVE: To report a case of systemic irinotecan toxicity following regional transarterial chemoembolization with drug-eluting beads loaded with irinotecan (DEBIRI-TACE) in a patient later found to have a homozygous mutation for UGT1A1*28.	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	231-237
25202035-1	2014	OBJECTIVE: To report a case of systemic irinotecan toxicity following regional transarterial chemoembolization with drug-eluting beads loaded with irinotecan (DEBIRI-TACE) in a patient later found to have a homozygous mutation for UGT1A1*28.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	231-237
25202035-7	2014	Patients with genetic polymorphisms of the genes encoding for the enzyme UGT1A1 may have increased incidence of irinotecan-associated toxicities because of decreased clearance of the active metabolite SN38 via the glucuronidation pathway.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
25217485-5	2014	Evaluation of PRAG formation by recombinant UDP-glucuronosyltransferase (UGT) isoforms and an inhibition study using HLHs as an enzyme source demonstrated that multiple UGT isoforms, including UGT1A1, UGT1A9, and UGT2B7, catalyzed probenecid acyl glucuronidation.	Probenecid	231-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	193-199
25877315-0	2015	[Association of UGT1A1 (*28, *60 and * 93) polymorphism with the adverse reactions of irinotecan chemotherapy in extensive stage small cell lung cancer].	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
25877315-1	2015	OBJECTIVE: To explore the correlation between UGT1A1 (*28, *60 and * 93) polymorphism and the adverse reactions in small cell lung cancer patients after irinotecan chemotherapy.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
25877315-9	2015	Further prospective study in a larger number of patients is needed to clarify the association between UGT1A1*28, UGT1A1* 93 and UGT1A1*60 polymorphism and adverse reactions of irinotecan, and to help clinicians in choosing a better therapeutic modality for personalized chemotherapy to improve curative effect and reduce adverse reactions.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
25151207-3	2014	METHODS: Nineteen SNPs in the ABCB1, NR1I2, UGT1A1, SLCO1B1 and CYP3A5 genes were examined in case patients with atazanavir/ritonavir-induced nephrolithiasis (n = 31) and controls (n = 47).	Ritonavir	124-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
25312789-6	2014	Of these subjects, 21% required a warfarin dose higher than 70 mg/week, which was associated with a BMI greater than 25 kg/m(2), use of warfarin antagonists, and the presence of the MDR1 3435T allele and UGT1A1(TA) 7 polymorphism.	Warfarin	34-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	204-210
25262300-4	2014	RESULTS: For UGT1A1, we found minor allele A of rs4148323 (G211A, UGT1A1*6) contributed to higher daily bilirubin levels on days 4-6 (with contributions to variations increasing from 4.8% to 12.3%), minor allele T of rs887829 (c-364t) contributed to lower daily bilirubin levels for days 6 and 7 (with contributions to variations increasing from 7.0% to 10.2%) (P &lt; .03 for all).	Bilirubin	262-271	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
25262300-7	2014	CONCLUSION: Bilirubin levels and changes during the middle and late parts of the first week were attributed to variants and haplotypes in UGT1A1.	Bilirubin	12-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
25086287-2	2014	The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 (UGT1A1) is solely responsible for clearing bilirubin from the blood and homozygosity for seven thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinaemia (Gilbert"s syndrome).	Bilirubin	115-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-70
25086287-2	2014	The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 (UGT1A1) is solely responsible for clearing bilirubin from the blood and homozygosity for seven thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinaemia (Gilbert"s syndrome).	Bilirubin	115-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
25086287-2	2014	The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 (UGT1A1) is solely responsible for clearing bilirubin from the blood and homozygosity for seven thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinaemia (Gilbert"s syndrome).	Bilirubin	115-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	238-244
25086287-2	2014	The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 (UGT1A1) is solely responsible for clearing bilirubin from the blood and homozygosity for seven thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinaemia (Gilbert"s syndrome).	thymine-adenine	167-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-70
25086287-2	2014	The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 (UGT1A1) is solely responsible for clearing bilirubin from the blood and homozygosity for seven thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinaemia (Gilbert"s syndrome).	thymine-adenine	167-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
25086287-2	2014	The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 (UGT1A1) is solely responsible for clearing bilirubin from the blood and homozygosity for seven thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinaemia (Gilbert"s syndrome).	thymine-adenine	167-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	238-244
25262300-1	2014	OBJECTIVE: To explore the effects of variants in Uridine Diphosphate Glucuronosyl Transferase 1A1 (UGT1A1) and Heme Oxygenase-1 (HMOX1) on daily physiological bilirubin levels and bilirubin changes during the first week after birth in Chinese newborns.	Bilirubin	159-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-97
25262300-1	2014	OBJECTIVE: To explore the effects of variants in Uridine Diphosphate Glucuronosyl Transferase 1A1 (UGT1A1) and Heme Oxygenase-1 (HMOX1) on daily physiological bilirubin levels and bilirubin changes during the first week after birth in Chinese newborns.	Bilirubin	159-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
25262300-2	2014	Both UGT1A1 and HMOX1 code rate-limiting enzymes in the bilirubin metabolism pathway.	Bilirubin	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
25262300-4	2014	RESULTS: For UGT1A1, we found minor allele A of rs4148323 (G211A, UGT1A1*6) contributed to higher daily bilirubin levels on days 4-6 (with contributions to variations increasing from 4.8% to 12.3%), minor allele T of rs887829 (c-364t) contributed to lower daily bilirubin levels for days 6 and 7 (with contributions to variations increasing from 7.0% to 10.2%) (P &lt; .03 for all).	Bilirubin	104-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25262300-4	2014	RESULTS: For UGT1A1, we found minor allele A of rs4148323 (G211A, UGT1A1*6) contributed to higher daily bilirubin levels on days 4-6 (with contributions to variations increasing from 4.8% to 12.3%), minor allele T of rs887829 (c-364t) contributed to lower daily bilirubin levels for days 6 and 7 (with contributions to variations increasing from 7.0% to 10.2%) (P &lt; .03 for all).	Bilirubin	104-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
25262300-4	2014	RESULTS: For UGT1A1, we found minor allele A of rs4148323 (G211A, UGT1A1*6) contributed to higher daily bilirubin levels on days 4-6 (with contributions to variations increasing from 4.8% to 12.3%), minor allele T of rs887829 (c-364t) contributed to lower daily bilirubin levels for days 6 and 7 (with contributions to variations increasing from 7.0% to 10.2%) (P &lt; .03 for all).	Carbon	76-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25262300-4	2014	RESULTS: For UGT1A1, we found minor allele A of rs4148323 (G211A, UGT1A1*6) contributed to higher daily bilirubin levels on days 4-6 (with contributions to variations increasing from 4.8% to 12.3%), minor allele T of rs887829 (c-364t) contributed to lower daily bilirubin levels for days 6 and 7 (with contributions to variations increasing from 7.0% to 10.2%) (P &lt; .03 for all).	Carbon	76-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
25262300-4	2014	RESULTS: For UGT1A1, we found minor allele A of rs4148323 (G211A, UGT1A1*6) contributed to higher daily bilirubin levels on days 4-6 (with contributions to variations increasing from 4.8% to 12.3%), minor allele T of rs887829 (c-364t) contributed to lower daily bilirubin levels for days 6 and 7 (with contributions to variations increasing from 7.0% to 10.2%) (P &lt; .03 for all).	Bilirubin	262-271	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25312789-9	2014	The UGT1A1(TA) 7 allele was positively correlated with the warfarin dose.	Warfarin	59-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
25312789-10	2014	CONCLUSION: CYP2C9*2, CYP2C9*3, VKORC1-1639G&gt;A, and APOE *epsilon4 were associated with lower warfarin doses, while MDR1 3435C&gt;T and UGT1A1(TA) n polymorphisms were associated with a requirement for higher doses.	Warfarin	97-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
25364403-3	2014	The current study demonstrates that rapamycin may enhance the chemopreventive effects of SFN on Caco-2 cells; this may be partially attributed to nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2)- and human pregnane X receptor (hPXR)-mediated UGT1A1, UGT1A8 and UGT1A10 induction.	Sirolimus	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	269-275
25394051-4	2014	Atazanavir (ATV) inhibits UGT1A1, thus increasing unconjugated BR levels, a distinctive feature of this drug.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
25473295-0	2014	FOLFIRI and regorafenib combination therapy with dose escalation of irinotecan as fourth-line treatment for patients with metastatic colon cancer according to UGT1A1 genotyping.	FOLFIRI regimen	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
25200497-1	2014	BACKGROUNDS AND AIMS: UDP-glucuronosyltransferase 1 A1 (UGT1A1) is an enzyme that transforms small lipophilic molecules into water-soluble and excretable metabolites.	Water	125-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-54
25200497-1	2014	BACKGROUNDS AND AIMS: UDP-glucuronosyltransferase 1 A1 (UGT1A1) is an enzyme that transforms small lipophilic molecules into water-soluble and excretable metabolites.	Water	125-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	181-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	181-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	181-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
25200497-9	2014	Quantitative analysis showed that sense mutation (including UGT1A1*6) and UGT1A1*28/*28, but not UGT1A1*60/*60 or UGT1A1*1/*28, was associated with increased serum total bilirubin (TB) levels.	Bilirubin	181-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
25200497-11	2014	CONCLUSIONS: This study identified four novel UGT1A1 coding variants, some of which were associated with increased serum TB levels.	Bilirubin	121-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
25394086-4	2014	ATV contributes to the decreased levels of UGT1A1, which may lead to elevations of indirect bilirubin, jaundice and even to therapy discontinuation.	Atazanavir Sulfate	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
25394086-4	2014	ATV contributes to the decreased levels of UGT1A1, which may lead to elevations of indirect bilirubin, jaundice and even to therapy discontinuation.	Bilirubin	92-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
25394086-19	2014	CONCLUSIONS: The risk of severe hyperbilirubinemia during ATV treatment is minimal for patients without UGT1A1*28 and no more than one additional risk factor and for patients with UGT1A1*28 and no additional risk factors; patients with homozygous genotype UGT1A1*28 are at the highest risk.	Atazanavir Sulfate	58-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
25394086-19	2014	CONCLUSIONS: The risk of severe hyperbilirubinemia during ATV treatment is minimal for patients without UGT1A1*28 and no more than one additional risk factor and for patients with UGT1A1*28 and no additional risk factors; patients with homozygous genotype UGT1A1*28 are at the highest risk.	Atazanavir Sulfate	58-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
25394086-19	2014	CONCLUSIONS: The risk of severe hyperbilirubinemia during ATV treatment is minimal for patients without UGT1A1*28 and no more than one additional risk factor and for patients with UGT1A1*28 and no additional risk factors; patients with homozygous genotype UGT1A1*28 are at the highest risk.	Atazanavir Sulfate	58-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
25192553-0	2014	Exploring the roles of UGT1A1 and UGT1A3 in oral clearance of GSK2190915, a 5-lipoxygenase-activating protein inhibitor.	3-(3-tert-butylsulfanyl-1-(4-(6-ethoxypyridin-3-yl)benzyl)-5-(5-methylpyridin-2-ylmethoxy)-1H-indol-2-yl)-2,2-dimethylpropionic acid	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
25473295-0	2014	FOLFIRI and regorafenib combination therapy with dose escalation of irinotecan as fourth-line treatment for patients with metastatic colon cancer according to UGT1A1 genotyping.	Irinotecan	68-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
25473295-1	2014	Here we report a case of metastatic colon cancer treated with 5-fluorouracil, leucovorin, and escalated doses of irinotecan (FOLFIRI) combined with regorafenib in the fourth-line setting after uridine diphosphate glucuronosyltransferase (UGT)1A1 genotyping analysis.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	238-245
25473295-1	2014	Here we report a case of metastatic colon cancer treated with 5-fluorouracil, leucovorin, and escalated doses of irinotecan (FOLFIRI) combined with regorafenib in the fourth-line setting after uridine diphosphate glucuronosyltransferase (UGT)1A1 genotyping analysis.	FOLFIRI regimen	125-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	238-245
25473295-1	2014	Here we report a case of metastatic colon cancer treated with 5-fluorouracil, leucovorin, and escalated doses of irinotecan (FOLFIRI) combined with regorafenib in the fourth-line setting after uridine diphosphate glucuronosyltransferase (UGT)1A1 genotyping analysis.	regorafenib	148-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	238-245
25473295-9	2014	FOLFIRI, with dose escalation of irinotecan according to UGT1A1 genotyping plus regorafenib appears to be a promising salvage therapy for patients with refractory metastatic colorectal cancer.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
25394051-4	2014	Atazanavir (ATV) inhibits UGT1A1, thus increasing unconjugated BR levels, a distinctive feature of this drug.	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
25105254-2	2014	Bilirubin is a potent endogenous antioxidant, and the UGT1A1*28 polymorphism is the main genetic cause of variation in plasma bilirubin in Western Europe.	Bilirubin	126-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
24910925-1	2014	AIM: To evaluate the impact of genetic polymorphisms in uridine 5"-glucuronosylytansferases UGT1A1 and UGT1A3 and iodothyronine-deiodinases types 1 and 2 on levothyroxine (T4 ; 3,5,3",5"-triiodo-L-thyronine) dose requirement for suppression of thyrotropin (TSH) secretion in patients with differentiated thyroid cancer (DTC).	Uridine	56-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
25162819-5	2014	Prolonged raltegravir elimination likely reflects low neonatal UGT1A1 enzyme activity and enterohepatic recirculation.	Raltegravir Potassium	10-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
25450281-1	2014	OBJECTIVE: The aim was to investigate the association between uridine diphosphate glucuronide transferase 1A1 (UGT1A1) gene promoter region polymorphism and irinotecan-related adverse effects and efficacy on recurrent and refractory small cell lung cancer (SCLC).	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-109
25450281-1	2014	OBJECTIVE: The aim was to investigate the association between uridine diphosphate glucuronide transferase 1A1 (UGT1A1) gene promoter region polymorphism and irinotecan-related adverse effects and efficacy on recurrent and refractory small cell lung cancer (SCLC).	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
25450281-4	2014	DNA was extracted from peripheral blood and direct sequencing method was employed to test UGT1A1FNx0128 polymorphism, thus analyzing the correlation between UGT1A1FNx0128 polymorphism and irinotecan-related side-effects and efficacy.	Irinotecan	188-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
25204339-8	2014	Overall, the reversible, unconjugated hyperbilirubinemia associated with faldaprevir may predominantly result from inhibition of bilirubin conjugation by UGT1A1, with inhibition of hepatic uptake of bilirubin also potentially playing a role.	faldaprevir	73-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
25204339-8	2014	Overall, the reversible, unconjugated hyperbilirubinemia associated with faldaprevir may predominantly result from inhibition of bilirubin conjugation by UGT1A1, with inhibition of hepatic uptake of bilirubin also potentially playing a role.	Bilirubin	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
25204339-8	2014	Overall, the reversible, unconjugated hyperbilirubinemia associated with faldaprevir may predominantly result from inhibition of bilirubin conjugation by UGT1A1, with inhibition of hepatic uptake of bilirubin also potentially playing a role.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
25319636-0	2014	Crigler-Najjar syndrome type II in a Chinese boy resulting from three mutations in the bilirubin uridine 5"-diphosphate-glucuronosyltransferase (UGT1A1) gene and a family genetic analysis.	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
25493567-11	2014	Conclusion: We identified a UGT1A1 promoter variant (rs2003569) associated with simvastatin efficacy.	Simvastatin	80-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
25319636-1	2014	BACKGROUND: The UGT1A1 gene encodes a responsible enzyme, UDP-glucuronosyltransferase1A1 (UGT1A1), for bilirubin metabolism.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
25319636-1	2014	BACKGROUND: The UGT1A1 gene encodes a responsible enzyme, UDP-glucuronosyltransferase1A1 (UGT1A1), for bilirubin metabolism.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-88
25319636-1	2014	BACKGROUND: The UGT1A1 gene encodes a responsible enzyme, UDP-glucuronosyltransferase1A1 (UGT1A1), for bilirubin metabolism.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
24709690-0	2014	The effect of the UGT1A1*28 allele on survival after irinotecan-based chemotherapy: a collaborative meta-analysis.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
25219630-7	2014	Capsaicin glucuronidation was significantly correlated with 3-O-glucuronidation of beta-estradiol (r = 0.637; p = 0.014) and with UGT1A1 protein levels (r = 0.616; p = 0.019) in a bank of individual HLMs (n = 14).	Capsaicin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
25219630-9	2014	UGT1A1, 1A9 and 2B7 contributed 30.3, 6.0 and 49.0% of total glucuronidation of capsaicin in pHLM, respectively.	Capsaicin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25219630-11	2014	CONCLUSION: Capsaicin was subjected to significant hepatic glucuronidation, wherein UGT1A1 and 2B7 were the main contributing enzymes.	Capsaicin	12-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-98
24620945-2	2014	The high levels of bilirubin could be related to the co-inheritance of Gilbert syndrome determined either by mutations of the coding region or by variation in the (TA)n motifs of the promoter region of the bilirubin UGT1A1 gene.	Bilirubin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	216-222
24620945-2	2014	The high levels of bilirubin could be related to the co-inheritance of Gilbert syndrome determined either by mutations of the coding region or by variation in the (TA)n motifs of the promoter region of the bilirubin UGT1A1 gene.	Bilirubin	206-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	216-222
24620945-5	2014	METHODS: The promoter region (TA)n motifs of the bilirubin UGT1A1 gene were analyzed in 104 beta thalassemia individuals.	Bilirubin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
24516079-1	2014	Hyperbilirubinaemia with or without jaundice is one of the side effects of atazanavir boosted with low-dose ritonavir (ATV/rit) related to the drug plasma levels, as a result of its metabolism by UGT1A1 - uridine diphosphate-glucuronosyl transferase.	Atazanavir Sulfate	75-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
24516079-1	2014	Hyperbilirubinaemia with or without jaundice is one of the side effects of atazanavir boosted with low-dose ritonavir (ATV/rit) related to the drug plasma levels, as a result of its metabolism by UGT1A1 - uridine diphosphate-glucuronosyl transferase.	Ritonavir	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
24516079-1	2014	Hyperbilirubinaemia with or without jaundice is one of the side effects of atazanavir boosted with low-dose ritonavir (ATV/rit) related to the drug plasma levels, as a result of its metabolism by UGT1A1 - uridine diphosphate-glucuronosyl transferase.	Atazanavir Sulfate	119-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
24516079-2	2014	Genotyping for UGT1A1*28 before initiation of antiretroviral therapy containing atazanavir may aid in identifying individuals at risk of hyperbilirubinaemia.	Atazanavir Sulfate	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
24516079-8	2014	Of the ATV/rit-treated patients, 14 were found to be carriers of the UGT1A1*28 variant (54%), and maximum serum bilirubin levels were significantly higher in the carrier population (4.71 vs. 2.69 mg/dL, p = 0.026).	Atazanavir Sulfate	7-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
24516079-8	2014	Of the ATV/rit-treated patients, 14 were found to be carriers of the UGT1A1*28 variant (54%), and maximum serum bilirubin levels were significantly higher in the carrier population (4.71 vs. 2.69 mg/dL, p = 0.026).	Ritonavir	11-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
24516079-8	2014	Of the ATV/rit-treated patients, 14 were found to be carriers of the UGT1A1*28 variant (54%), and maximum serum bilirubin levels were significantly higher in the carrier population (4.71 vs. 2.69 mg/dL, p = 0.026).	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
26692748-11	2014	In addition, if 7-hydroxymitragynine is to be taken with other drugs that are highly metabolized by UGT1A1, there is a possibility of drug-drug interaction to occur.	7-hydroxymitragynine	16-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
24709690-1	2014	To date, studies of irinotecan pharmacogenetics have mostly focused on the effect of the UGT1A1*28 allele on irinotecan-related toxicity.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
24709690-1	2014	To date, studies of irinotecan pharmacogenetics have mostly focused on the effect of the UGT1A1*28 allele on irinotecan-related toxicity.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
24709690-2	2014	However, the clinical utility of routine UGT1A1*28 genotyping to pre-emptively adjust irinotecan dosage is dependent upon whether UGT1A1*28 also affects patient survival following irinotecan therapy.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
24709690-2	2014	However, the clinical utility of routine UGT1A1*28 genotyping to pre-emptively adjust irinotecan dosage is dependent upon whether UGT1A1*28 also affects patient survival following irinotecan therapy.	Irinotecan	180-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
24709690-4	2014	A systematic review and meta-analysis of both published and unpublished data were performed to summarize the available evidence of the relationship between the UGT1A1*28 allele and patient survival related to irinotecan therapy.	Irinotecan	209-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
25260839-0	2014	Influence of UGT1A1 gene methylation level in colorectal cancer cells on the sensitivity of the chemotherapy drug CPT-11.	Irinotecan	114-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25285015-0	2014	Clinical significance of UGT1A1 gene polymorphisms on irinotecan-based regimens as the treatment in metastatic colorectal cancer.	Irinotecan	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
25285015-1	2014	PURPOSE: The primary aim of this research was to investigate the association between uridine diphosphate glucuronosyltransferase (UGT)1A1 gene polymorphisms and the toxicities of irinotecan-based regimens in Chinese patients with metastatic colorectal cancer.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-137
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25210794-11	2014	However, HT29 cells became sensitized to the drug, and HSP90 client proteins were destabilized by ganetespib upon siRNA-mediated UGT1A knockdown.	STA 9090	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-134
25210794-14	2014	We conclude that CRC cell-expressed UGT1A inactivates ganetespib and other resorcinolic Hsp90 inhibitors by glucuronidation, which renders the drugs unable to inhibit Hsp90 and thereby abrogates their biological activity.	STA 9090	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-41
25210794-15	2014	UGT1A levels in tumor tissues may be a suitable predictive biomarker to stratify CRC patients for ganetespib treatment.	STA 9090	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-5
25209391-0	2014	Glucose induces intestinal human UDP-glucuronosyltransferase (UGT) 1A1 to prevent neonatal hyperbilirubinemia.	Glucose	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-70
25209391-2	2014	This study experimentally investigated whether additional glucose treatments induce the bilirubin-metabolizing enzyme--UDP-glucuronosyltransferase (UGT) 1A1--to prevent the onset of neonatal hyperbilirubinemia.	Glucose	58-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-156
25209391-2	2014	This study experimentally investigated whether additional glucose treatments induce the bilirubin-metabolizing enzyme--UDP-glucuronosyltransferase (UGT) 1A1--to prevent the onset of neonatal hyperbilirubinemia.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-156
25209391-4	2014	In this study, UGT1A1 expression levels were determined in the liver and small intestine of neonatal hUGT1 mice that were orally treated with glucose.	Glucose	142-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-106
25209391-5	2014	In the hUGT1 mice, glucose induced UGT1A1 in the small intestine, while it did not affect the expression of UGT1A1 in the liver.	Glucose	19-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	7-12
25209391-6	2014	UGT1A1 was also induced in the human intestinal Caco-2 cells when the cells were cultured in the presence of glucose.	Glucose	109-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25209391-8	2014	Adequate calorie intake would lead to the sufficient expression of UGT1A1 in the small intestine to reduce serum bilirubin levels.	Bilirubin	113-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Glucuronides	4-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Estradiol	20-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Serotonin	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Propofol	54-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Zidovudine	64-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Zidovudine	92-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
24752421-6	2014	The glucuronides of estradiol, imipramine, serotonin, propofol, 3"-azido-3"-deoxythymidine (AZT) and morphine, selective substrates of human UGT1A1, 1A4, 1A6, 1A9 and 2B7 (AZT and morphine), respectively, were measured using LC-MS/MS.	Morphine	101-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25044472-7	2014	UGT1A1, 1A3 and 1A10 showed activities on both 3"-OH and 7-OH, whereas UGT1A7, 1A8, 1A9, and 2B7 were only capable of catalyzing 3"-OH glucuronidation of calycosin.	3"-oh	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25044472-7	2014	UGT1A1, 1A3 and 1A10 showed activities on both 3"-OH and 7-OH, whereas UGT1A7, 1A8, 1A9, and 2B7 were only capable of catalyzing 3"-OH glucuronidation of calycosin.	7,3'-dihydroxy-4'-methoxyisoflavone	154-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25044472-9	2014	UGT1A1 showed the highest activity towards 7-OH glucuronidation (Clint, 224.34 muL/min/mg protein), which was comparable to its activity on 3"-OH glucuronidation (Clint, 203.82 muL/min/mg protein).	7-oh	43-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25044472-10	2014	Propofol (UGT1A9 inhibitor) produced a complete inhibition of 3"-glucuronide formation accompanied by an increase of 7-glucuronide in HLMs, while bilirubin (UGT1A1 inhibitor) only partially (~60%) inhibited the 7-OH glucuronidation.	Bilirubin	146-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
25260839-1	2014	OBJECTIVE: To study the influence of the methylation level of UGT1A1 gene related to CPT-11 metabolic enzymes in colorectal cancer cells on the sensitivity of chemotherapy drugs.	Irinotecan	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25260839-6	2014	CONCLUSIONS: The cytotoxicity of CPT-11 to colorectal cancer cells has a negative correlation with UGT1A1 expression, and positive correlation with CES2 and GUSB.	Irinotecan	33-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
25260839-7	2014	The specific silencing UGT1A1 gene of siRNA could significantly increase the sensitivity of CPT-11 to the chemotherapy of colorectal cancer cells.	Irinotecan	92-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
25260839-8	2014	UGT1A1 methylation was an important factor affecting the chemosensitivity of CPT-11.	Irinotecan	77-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24954688-4	2014	Kinetics studies were conducted to evaluate the K i values and mechanism(s) of the inhibition of CYP2E1, CYP3A4, UGT1A1 and UGT1A9 by p-cresol.	4-cresol	134-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
24954688-6	2014	p-Cresol was the most potent individual inhibitor, producing &gt;50% inhibition of CYP2E1, CYP3A4, UGT1A1, UGT1A9 and UGT2B7 at a concentration of 100 muM.	4-cresol	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
24954688-9	2014	K i values for p-cresol inhibition of human liver microsomal CYP2E1, CYP3A4 and UGT1A1 ranged from 43 to 89 muM.	4-cresol	15-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
24635759-4	2014	Among 12 recombinant human UDP-glucuronosyltransferases (UGTs), UGT1A1, UGT1A8, UGT1A9, and UGT1A10 showed catalyzing activity toward leonurine glucuronidation.	leonurine	134-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
25092941-3	2014	UGT1A1 is the rate-limiting enzyme in bilirubin"s metabolism.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25054039-0	2014	Clinical usefulness of testing for UDP glucuronosyltransferase 1 family, polypeptide A1 polymorphism prior to the inititation of irinotecan-based chemotherapy.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-87
25054039-1	2014	An association between UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) polymorphisms and irinotecan-induced neutropenia has been previously reported.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-75
25054039-1	2014	An association between UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) polymorphisms and irinotecan-induced neutropenia has been previously reported.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
24635759-6	2014	Both chemical inhibition study and correlation study demonstrated that leonurine glucuronidation activities in HLMs had significant relationship with UGT1A1 activities.	leonurine	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
24635759-8	2014	UGT1A1 was principal enzyme that responsible for leonurine glucuronidation in human liver and intestine microsomes.	leonurine	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24650397-10	2014	CONCLUSION: One-half of the infants with BMJ were homozygous UGT1A1*6 and exhibited a serum bilirubin concentration significantly greater than other genotypes.	Bilirubin	92-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
24928535-6	2014	The up-regulation of MDR1 and UGT1A1 by anticancer agents was further enhanced in the presence of CITCO.	6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime	98-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
24462762-3	2014	The study group received irinotecan dose escalation based on UGT1A1 genotyping whereas the control group did not.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
24462762-5	2014	The clinical response rate of patients with mCRC treated with FOLFIRI plus bevacizumab under UGT1A1 genotyping and irinotecan dose escalation was significantly better than that of those without these prospective tests and dose escalation (P = 0.028).	FOLFIRI regimen	62-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24462762-8	2014	Patients with mCRC undergoing UGT1A1 genotyping may receive escalated doses of irinotecan to obtain a better clinical response/outcome with comparable toxicities.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
24865931-4	2014	Genetic polymorphisms of the UGT1A1 promoter, specifically the -3279 T G phenobarbital responsive enhancer module (rs4124874) and (TA)7 dinucleotide repeat (rs8175347) as well as the coding region variants (rs2306283 and rs4149056) of the OATP2 gene were significantly higher among the cases than the controls.	Phenobarbital	73-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
24865931-7	2014	This study demonstrates that UGT1A1 and OATP2 polymorphisms were associated with altered bilirubin metabolism and could be genetic risk factors for neonatal hyperbilirubinemia.	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
24785582-1	2014	BACKGROUND: Gilbert"s syndrome is one of the most common metabolic syndromes in the human population characterised by mild unconjugated hyperbilirubinemia resulting from reduced activity of the bilirubin conjugating enzyme UDP-glucuronosyltransferase (UGT1A1).	Bilirubin	141-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	252-258
24958824-0	2014	Dose-finding and pharmacokinetic study to optimize the dosing of irinotecan according to the UGT1A1 genotype of patients with cancer.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-1	2014	PURPOSE: The risk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-1	2014	PURPOSE: The risk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-1	2014	PURPOSE: The risk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	178-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-14	2014	CONCLUSION: The UGT1A1*28 genotype can be used to individualize dosing of irinotecan.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
24837423-3	2014	The hypothesis of a system is supported by (i) coordinate regulation of subsets of these enzyme families and transporters by transcription factors including the AhR, and (ii) feedback loops between endobiotic AhR agonists and substrates of major catabolic target genes/proteins; for example, 6-formylindolo[3,2-b]carbazole as substrate of CYP1A1, and bilirubin, as substrate of UGT1A1.	6-formylindolo(3,2-b)carbazole	292-322	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	378-384
24837423-3	2014	The hypothesis of a system is supported by (i) coordinate regulation of subsets of these enzyme families and transporters by transcription factors including the AhR, and (ii) feedback loops between endobiotic AhR agonists and substrates of major catabolic target genes/proteins; for example, 6-formylindolo[3,2-b]carbazole as substrate of CYP1A1, and bilirubin, as substrate of UGT1A1.	Bilirubin	351-360	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	378-384
24650397-2	2014	STUDY DESIGN: UGT1A1 gene allelic variation was analyzed in 170 Japanese infants with BMJ with polymerase chain reaction-direct sequencing, and their genotypes compared with serum bilirubin concentrations.	Bilirubin	180-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
24650397-12	2014	Previous finding have demonstrated that 5beta-pregnane-3alpha,20beta-diol present in breast milk inhibits p.G71R-UGT1A1 bilirubin glucuronidation activity.	5beta-pregnane-3alpha	40-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
24650397-12	2014	Previous finding have demonstrated that 5beta-pregnane-3alpha,20beta-diol present in breast milk inhibits p.G71R-UGT1A1 bilirubin glucuronidation activity.	20beta-diol	62-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
24650397-12	2014	Previous finding have demonstrated that 5beta-pregnane-3alpha,20beta-diol present in breast milk inhibits p.G71R-UGT1A1 bilirubin glucuronidation activity.	Bilirubin	120-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
24901842-2	2014	The UGT1A1*28 polymorphism (TA repeats in the promoter region) is a major determinant of bilirubin levels and recent evidence suggests that raised adiposity may also be a contributing factor.	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
24857157-7	2014	Subsequently, the mRNA levels of AHR-targeting drug-metabolizing enzymes (CYP1A1, UGT1A1, and ABCG 2) and the protein level of CYP1A1 in HepG2 cells were shown to be increased by 6-shogaol.	shogaol	179-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
24901842-3	2014	We aimed to study the interaction between UGT1A1 polymorphism, hematological and anthropometric variables with total bilirubin levels in young individuals.	Bilirubin	117-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
24901842-12	2014	UGT1A1 polymorphism and body fat percentage were the main factors affecting bilirubin levels within obese patients (linear regression analysis).	Bilirubin	76-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24901842-13	2014	CONCLUSION: In obese children and adolescents, body fat composition and UGT1A1 polymorphism are independent determinants of total bilirubin levels.	Bilirubin	130-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
24977443-0	2014	[Interest of UGT1A1 genotyping within digestive cancers treatment by irinotecan].	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
24977443-2	2014	Its anticancer activity results from its bioactivation into SN-38 metabolite, which is cleared through glucuronidation by the hepatic enzyme uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-188
24977443-2	2014	Its anticancer activity results from its bioactivation into SN-38 metabolite, which is cleared through glucuronidation by the hepatic enzyme uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
24977443-9	2014	The existence of a French laboratories network performing this test in clinical routine makes it possible to generalize UGT1A1 deficiency screening, so as to guarantee equal access to safe treatment and optimized irinorecan-based therapy for the many patients receiving irinotecan-based therapy in advanced colorectal cancer.	irinorecan	213-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
24977443-9	2014	The existence of a French laboratories network performing this test in clinical routine makes it possible to generalize UGT1A1 deficiency screening, so as to guarantee equal access to safe treatment and optimized irinorecan-based therapy for the many patients receiving irinotecan-based therapy in advanced colorectal cancer.	Irinotecan	270-280	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
24777631-6	2014	Rifampicin is also an inducer of the uridine diphosphate glucuronosyltransferase (UGT) 1A1 enzymes and interferes with drugs, such as integrase inhibitors, that are metabolized by this metabolic pathway.	Rifampin	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-90
25141892-0	2014	UGT1A1*28 polymorphisms: a potential pharmacological biomarker of irinotecan-based chemotherapies in colorectal cancer.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24932285-0	2014	Association between the low-dose irinotecan regimen-induced occurrence of grade 4 neutropenia and genetic variants of UGT1A1 in patients with gynecological cancers.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-171
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	71-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-171
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	71-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179
24932285-6	2014	The association between the absolute neutrophil count (ANC) nadir values, the total dose of CPT-11 and the genotypes of UGT1A1 or ABCG2 was studied.	Irinotecan	92-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
24932285-12	2014	In conclusion, the UGT1A1*6/*28 and *6/*6 genotypes were found to be associated with the occurrence of severe neutropenia in the low-dose CPT-11 regimen for gynecological cancers.	Irinotecan	138-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
24932285-13	2014	This finding indicates that the determination of UGT1A1 variants may be as useful in CPT-11 chemotherapy for gynecological conditions as it is in colorectal and lung cancer patients treated with this drug.	Irinotecan	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
24453052-10	2014	A comprehensive study of the influence of UGT1A1 polymorphisms on the risk of irinotecan-induced toxicity is necessary for optimal use of irinotecan treatment.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
24453052-10	2014	A comprehensive study of the influence of UGT1A1 polymorphisms on the risk of irinotecan-induced toxicity is necessary for optimal use of irinotecan treatment.	Irinotecan	138-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
24375494-0	2014	Analysis of flavonoids regulating the expression of UGT1A1 via xenobiotic receptors in intestinal epithelial cells.	Flavonoids	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
24834123-2	2014	Our purpose was to study the association between UGT1A1*28, UGT1A7*2, and UGT1A7*3 polymorphisms and irinotecan toxicity in Greek patients receiving low-dose weekly irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
24375494-2	2014	A screening assay using real-time PCR showed that baicalein and 3-hydroxyflavone induced human UGT1A1 mRNA expression in LS180 cells.	baicalein	50-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
24375494-2	2014	A screening assay using real-time PCR showed that baicalein and 3-hydroxyflavone induced human UGT1A1 mRNA expression in LS180 cells.	3-hydroxyflavone	64-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
24375494-4	2014	The results indicated that baicalein and 3-hydroxyflavone increased the transcriptional activity of UGT1A1 via AhR and PXR, respectively.	baicalein	27-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
24375494-4	2014	The results indicated that baicalein and 3-hydroxyflavone increased the transcriptional activity of UGT1A1 via AhR and PXR, respectively.	3-hydroxyflavone	41-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
24375494-7	2014	These results elucidate the molecular mechanism of flavonoid-induced UGT1A1 gene expression via xenobiotic receptors in the intestines.	Flavonoids	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
24598415-6	2014	Regulation of phase II rather than phase I metabolic enzymes was implicated mechanistically: raloxifene and DMA were observed to upregulate sulfotransferase (SULT 1E1) and glucuronidase (UGT 1A1).	Raloxifene Hydrochloride	93-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-194
24598415-6	2014	Regulation of phase II rather than phase I metabolic enzymes was implicated mechanistically: raloxifene and DMA were observed to upregulate sulfotransferase (SULT 1E1) and glucuronidase (UGT 1A1).	desmethylarzoxifene	108-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-194
23981182-3	2014	METHODS: We have investigated the UGT1A1 polymorphism frequency and its relation to severity of hyperbilirubinemia and jaundice duration among 220 exclusively breastfed term newborns; 57 of them with non-physiologic hyperbilirubinemia (NH), and 163 with BMJ, and in 187 healthy controls.	(12R)-12-methyltetradecanoic acid	254-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
24382596-0	2014	Pharmacokinetics, safety, and efficacy of FOLFIRI plus bevacizumab in Japanese colorectal cancer patients with UGT1A1 gene polymorphisms.	FOLFIRI regimen	42-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
24382596-1	2014	Previous reports of the influence of UGT1A1 gene polymorphisms on the pharmacokinetics of irinotecan metabolism have not assessed Asian patients treated with FOLFIRI plus bevacizumab for advanced and recurrent colorectal cancer.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
24627218-5	2014	In addition, inhibition of UDP-glucuronosyltransferase 1A1 (UGT1A1) variants by lenalidomide was also assessed.	Lenalidomide	80-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-58
24519753-0	2014	Associations between UGT1A1*6 or UGT1A1*6/*28 polymorphisms and irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	64-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
24519753-2	2014	Many studies have demonstrated that patients bearing UGT1A1*28 have a higher risk of severe neutropenia on toxicity of irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
24553666-5	2014	Recombinant UGT enzymes (UGT1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B10, 2B15) were screened for their activity towards ethanol, and kinetic data were then established for all enzymes.	Ethanol	111-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
24627218-5	2014	In addition, inhibition of UDP-glucuronosyltransferase 1A1 (UGT1A1) variants by lenalidomide was also assessed.	Lenalidomide	80-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
24519753-4	2014	Some researches reported that UGT1A1*28 and/or UGT1A1*6 could predict irinotecan-induced toxicities in Asian populations, but controversial conclusions still remained.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
24519753-4	2014	Some researches reported that UGT1A1*28 and/or UGT1A1*6 could predict irinotecan-induced toxicities in Asian populations, but controversial conclusions still remained.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-109
24519753-5	2014	This study aims to investigate the association between UGT1A1 gene polymorphisms *6, *6/*28 and irinotecan-related neutropenia in Asian cancer patients receiving irinotecan regimen chemotherapy.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24519753-5	2014	This study aims to investigate the association between UGT1A1 gene polymorphisms *6, *6/*28 and irinotecan-related neutropenia in Asian cancer patients receiving irinotecan regimen chemotherapy.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24519753-6	2014	EXPERIMENTAL DESIGN: Meta-analyses were done to assess the relationship between UGT1A1*6 or UGT1A1*6/*28 and irinotecan-induced neutropenia.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
24519753-6	2014	EXPERIMENTAL DESIGN: Meta-analyses were done to assess the relationship between UGT1A1*6 or UGT1A1*6/*28 and irinotecan-induced neutropenia.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
24519753-9	2014	CONCLUSIONS: In conclusion, the UGT1A1*6 and UGT1A1*6/*28 genotypes were associated with an increased risk of irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
24519753-9	2014	CONCLUSIONS: In conclusion, the UGT1A1*6 and UGT1A1*6/*28 genotypes were associated with an increased risk of irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	179-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-109
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	179-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
23605141-2	2014	The active metabolite of CPT-11, 7-ethyl-10-hydroxycamptothecin (SN-38) was glucuronidated (SN-38G) by UGT1A1.	cpt-11, 7-ethyl-10-hydroxycamptothecin	25-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
23605141-2	2014	The active metabolite of CPT-11, 7-ethyl-10-hydroxycamptothecin (SN-38) was glucuronidated (SN-38G) by UGT1A1.	Irinotecan	65-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
23605141-2	2014	The active metabolite of CPT-11, 7-ethyl-10-hydroxycamptothecin (SN-38) was glucuronidated (SN-38G) by UGT1A1.	Irinotecan	92-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
23605141-4	2014	Several studies have suggested that the dose of CPT-11 should be decreased in patients homozygous for UGT1A1*6 or UGT1A1*28, or double heterozygotes (*6/*28).	Irinotecan	48-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
23605141-4	2014	Several studies have suggested that the dose of CPT-11 should be decreased in patients homozygous for UGT1A1*6 or UGT1A1*28, or double heterozygotes (*6/*28).	Irinotecan	48-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	13-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	13-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	13-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	Irinotecan	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	Irinotecan	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	Irinotecan	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	30-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	30-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	30-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	Irinotecan	30-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	Irinotecan	30-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	Irinotecan	30-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
23609856-0	2014	Association between severe toxicity of nilotinib and UGT1A1 polymorphisms in Japanese patients with chronic myelogenous leukemia.	nilotinib	39-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
23609856-2	2014	The UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphism UGT1A1*28 (*28)/*28 has been linked to an increased risk of hyperbilirubinemia in patients with CML who receive nilotinib.	nilotinib	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-35
23609856-2	2014	The UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphism UGT1A1*28 (*28)/*28 has been linked to an increased risk of hyperbilirubinemia in patients with CML who receive nilotinib.	nilotinib	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
23609856-2	2014	The UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphism UGT1A1*28 (*28)/*28 has been linked to an increased risk of hyperbilirubinemia in patients with CML who receive nilotinib.	nilotinib	170-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
23609856-3	2014	Beside *28, UGT1A1*6 (*6) is another important variant allele in Japanese patients because it is associated with adverse events of irinotecan, metabolized by UGT1A1.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23609856-3	2014	Beside *28, UGT1A1*6 (*6) is another important variant allele in Japanese patients because it is associated with adverse events of irinotecan, metabolized by UGT1A1.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
23609856-4	2014	We retrospectively investigated the association between severe toxicity of nilotinib and UGT1A1 polymorphisms (*6 and*28) in Japanese patients with CML.	nilotinib	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
23609856-9	2014	CONCLUSION: These findings suggest that UGT1A1 polymorphisms are important determinants of severe toxicity of nilotinib in Japanese patients.	nilotinib	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
24525562-0	2014	Simultaneous determination of bilirubin and its glucuronides in liver microsomes and recombinant UGT1A1 enzyme incubation systems by HPLC method and its application to bilirubin glucuronidation studies.	Bilirubin	30-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
24525562-1	2014	Bilirubin, an important endogenous substances and liver function index in humans, is primarily eliminated via UGT1A1-catalyzed glucuronidation.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
24525562-8	2014	Furthermore, we established stable, reliable in vitro incubation systems and optimized the incubation conditions to characterize the kinetics of bilirubin glucuronidation by RLM, HLM and UGT1A1, respectively.	Bilirubin	145-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
24525562-10	2014	Bilirubin glucuronidation obeyed the Hill equation by RLM and the Michaelis-Menten equation by HLM and UGT1A1 in the range of substrate concentration selected, respectively.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
24525562-11	2014	In addition, the relative proportions between BDG and BMGs were in connection with enzyme sources (e.g. RLM, HLM and UGT1A1) and bilirubin concentration.	O(6)-n-butyldeoxyguanosine	46-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
23529007-0	2014	Association of UGT1A1*28 polymorphisms with irinotecan-induced toxicities in colorectal cancer: a meta-analysis in Caucasians.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
23529007-1	2014	A meta-analysis in Caucasians was conducted to investigate the possible association of uridine diphosphate glucuronosyltransferase (UGT) 1A1 gene polymorphisms with irinotecan (IRI)-induced neutropenia and diarrhoea in colorectal cancer (CRC).	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-140
23529007-8	2014	In subgroup meta-analysis, the higher incidence of diarrhoea in UGT1A1*28/*28 patients was limited to studies where when IRI was given at higher doses (OR=2.37, 95% CI: 1.39-4.04; P=0.002) or combined with 5-fluorouracil (FU or analogue) (OR=1.78, 95% CI: 1.16-2.75; P=0.009).	Fluorouracil	206-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
23529007-10	2014	IRI-combined 5-FU (or analogue) and a high-dose IRI therapy enhance IRI-induced diarrhoea among patients bearing the UGT1A1*28 allele.	Fluorouracil	13-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
24407487-4	2014	The (GT)n and (TA)n dinucleotide variations in heme oxygenase 1 (HMOX1) and bilirubin UDP-glucuronosyl transferase (UGT1A1) gene promoters were determined by fragment analysis.	Dinucleoside Phosphates	20-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
24557078-7	2014	By multivariate analysis, higher peak on-treatment bilirubin levels were found to be associated with the UGT1A1 rs887829 T allele (P=6.4x10(-12)), higher baseline hemoglobin levels (P=4.9x10(-13)), higher baseline bilirubin levels (P=6.7x10(-12)), and slower plasma atazanavir clearance (P=8.6x10(-11)).	Bilirubin	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
24557078-11	2014	CONCLUSION: Atazanavir-associated hyperbilirubinemia is best predicted by considering UGT1A1 genotype, baseline bilirubin level, and baseline hemoglobin level in combination.	Atazanavir Sulfate	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
24557078-11	2014	CONCLUSION: Atazanavir-associated hyperbilirubinemia is best predicted by considering UGT1A1 genotype, baseline bilirubin level, and baseline hemoglobin level in combination.	Bilirubin	39-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
24690955-2	2014	Bilirubin is produced by heme oxygenase-1 (HO-1), catalyzed by UDP-glucuronosyltransferase (UGT1A1), and has potential as an antioxidant.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
24690955-8	2014	Post-transplant 1-year bilirubin level was higher in 6/7 or 7/7 carriers compared with 6/6 homozygotes in terms of the UGT1A1*28 polymorphism (6/6 vs. 6/7 vs. 7/7: 0.71 +- 0.27 vs. 1.06 +- 0.36 vs. 1.10 +- 0.45 mg/dL, P&lt;0.001).	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
24690955-12	2014	CONCLUSIONS: The UGT1A1*28 polymorphism is associated with changes in serum bilirubin and with graft outcome after kidney transplantation.	Bilirubin	76-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
24066723-2	2014	Nilotinib, a tyrosine kinase inhibitor, could potently inhibit SN-38 glucuronidation mainly catalyzed by UDP-glucuronosyltransferase (UGT) 1A1.	nilotinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-142
24066723-2	2014	Nilotinib, a tyrosine kinase inhibitor, could potently inhibit SN-38 glucuronidation mainly catalyzed by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-142
24066723-3	2014	This study was designed to investigate whether nilotinib can be used as a selective inhibitor of UGT1A1 in human liver.	nilotinib	47-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
24066723-5	2014	Assays with recombinant UGTs indicated that nilotinib could strongly inhibit the activity of UGT1A1 and decreased the activity of extra-hepatic UGT1A7 to a much lesser extent.	nilotinib	44-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24066723-6	2014	The inhibition on 4-methylumbelliferone (4Mu) glucuronidation by recombinant UGT1A1 obeyed competitive inhibition mechanism, with a kinetic constants (Ki) value of 0.17 muM.	Hymecromone	18-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
24066723-7	2014	Assays with human liver microsomes (HLM) demonstrated that nilotinib could selectively inhibit estradiol-3-O-glucuronidation (E2-3-O-glucuronidation), a probe reaction of UGT1A1.	nilotinib	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
24066723-11	2014	Given that UGT1A7 is an extra-hepatic enzyme, this study indicates that nilotinib can be used as a selective inhibitor of UGT1A1 in human liver.	nilotinib	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
23996546-5	2014	The bergenin glucuronosyltransferase activities in HLMs and UGT1A1 were inhibited by phenylbutazone, estradiol and bilirubin.	Phenylbutazone	85-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
23996546-5	2014	The bergenin glucuronosyltransferase activities in HLMs and UGT1A1 were inhibited by phenylbutazone, estradiol and bilirubin.	Estradiol	101-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
23996546-5	2014	The bergenin glucuronosyltransferase activities in HLMs and UGT1A1 were inhibited by phenylbutazone, estradiol and bilirubin.	Bilirubin	115-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
24448639-0	2014	UGT1A1*6 polymorphisms are correlated with irinotecan-induced toxicity: a system review and meta-analysis in Asians.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	5-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
24897286-2	2014	This study comprehensively investigates the effects of UGT1A1 and UGT1A9 genetic polymorphism on SN-38 glucuronidation activity.	Irinotecan	97-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24897286-5	2014	The number of UGT1A1 reduced function alleles was associated with decreased SN-38G formation rates and UGT1A protein levels.	Irinotecan	76-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
24897286-8	2014	CONCLUSION: UGT1A1 genetic polymorphisms have a more important function in human liver SN-38 glucuronidation activity than UGT1A9.	Irinotecan	87-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
24696866-7	2014	Elvitegravir undergoes extensive primary metabolism by hepatic and intestinal cytochrome P450 3A (CYP3A) and secondary metabolism by UDP-glucuronosyltransferase 1-1 and 1-3 (UGT1A1/3).	elvitegravir	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
24407487-7	2014	Serum bilirubin levels were significantly lower in patients with CD within all UGT1A1*28 genotypes (P &lt; 0.05).	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
24407487-11	2014	UGT1A1*28 allele homozygosity, responsible for higher bilirubin levels, seems to be an important modifier of CD manifestation.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24318863-5	2014	Target genes were XPD-751, GSTP-1-105, XRCC1-399 for oxaliplatin, UGT1A1 for irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
24399855-6	2014	For UGT1A1, this repression correlated with significantly reduced metabolism of raloxifene into raloxifene-6-glucuronide (ral-6-gluc; P &lt; 0.01) and raloxifene-4"-glucuronide (ral-4"-gluc; P &lt; 0.01).	Raloxifene Hydrochloride	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
24399855-6	2014	For UGT1A1, this repression correlated with significantly reduced metabolism of raloxifene into raloxifene-6-glucuronide (ral-6-gluc; P &lt; 0.01) and raloxifene-4"-glucuronide (ral-4"-gluc; P &lt; 0.01).	Raloxifene 6-Glucuronide	96-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
23886114-3	2014	Genome-wide association studies have shown significant association of OATP1B1 and UGT1A1 with elevations of unconjugated bilirubin, and OATP1B1 inhibition data correlated with clinical unconjugated hyperbilirubinemia for several compounds.	Bilirubin	121-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
24399855-6	2014	For UGT1A1, this repression correlated with significantly reduced metabolism of raloxifene into raloxifene-6-glucuronide (ral-6-gluc; P &lt; 0.01) and raloxifene-4"-glucuronide (ral-4"-gluc; P &lt; 0.01).	ral-6-gluc	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
24399855-6	2014	For UGT1A1, this repression correlated with significantly reduced metabolism of raloxifene into raloxifene-6-glucuronide (ral-6-gluc; P &lt; 0.01) and raloxifene-4"-glucuronide (ral-4"-gluc; P &lt; 0.01).	Raloxifene 4'-Glucuronide	151-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
24399855-6	2014	For UGT1A1, this repression correlated with significantly reduced metabolism of raloxifene into raloxifene-6-glucuronide (ral-6-gluc; P &lt; 0.01) and raloxifene-4"-glucuronide (ral-4"-gluc; P &lt; 0.01).	ral-4"-gluc	178-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
24308720-0	2014	The association of UGT1A1*6 and UGT1A1*28 with irinotecan-induced neutropenia in Asians: a meta-analysis.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
24587300-0	2014	Serum bilirubin concentration in healthy adult North-Europeans is strictly controlled by the UGT1A1 TA-repeat variants.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24587300-1	2014	The major enzyme responsible for the glucuronidation of bilirubin is the uridine 5"-diphosphoglucose glucuronosyltransferase A1 (UGT1A1) enzyme, and genetic variation in the UGT1A1 gene is reported to influence the bilirubin concentration in the blood.	Bilirubin	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
24587300-1	2014	The major enzyme responsible for the glucuronidation of bilirubin is the uridine 5"-diphosphoglucose glucuronosyltransferase A1 (UGT1A1) enzyme, and genetic variation in the UGT1A1 gene is reported to influence the bilirubin concentration in the blood.	Bilirubin	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
24587300-1	2014	The major enzyme responsible for the glucuronidation of bilirubin is the uridine 5"-diphosphoglucose glucuronosyltransferase A1 (UGT1A1) enzyme, and genetic variation in the UGT1A1 gene is reported to influence the bilirubin concentration in the blood.	uridine 5"-	73-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
24587300-1	2014	The major enzyme responsible for the glucuronidation of bilirubin is the uridine 5"-diphosphoglucose glucuronosyltransferase A1 (UGT1A1) enzyme, and genetic variation in the UGT1A1 gene is reported to influence the bilirubin concentration in the blood.	Bilirubin	215-224	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
24587300-1	2014	The major enzyme responsible for the glucuronidation of bilirubin is the uridine 5"-diphosphoglucose glucuronosyltransferase A1 (UGT1A1) enzyme, and genetic variation in the UGT1A1 gene is reported to influence the bilirubin concentration in the blood.	Bilirubin	215-224	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
24587300-5	2014	We found significant odds ratios for high bilirubin level for all the selected UGT1A1 variants.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
24587300-6	2014	However, in stepwise multivariate logistic regression analysis of all genetic variants together with age, sex, country of origin and fasting time, the repeat variants of UGT1A1 TA6&gt;TA7 and SLCO1B3 rs2117032 T&gt;C were the only variants significantly associated with higher bilirubin concentrations.	Bilirubin	277-286	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
24587300-8	2014	Among individuals heterozygous for the TA7-repeat, a low frequent UGT1A1-diplotype harboring the rs7564935 G-variant was associated with higher bilirubin levels.	Bilirubin	144-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
24308720-0	2014	The association of UGT1A1*6 and UGT1A1*28 with irinotecan-induced neutropenia in Asians: a meta-analysis.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
24308720-1	2014	BACKGROUND: The UGT1A1*28 polymorphism is known as a biomarker of irinotecan-induced neutropenia in Caucasians.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
24308720-5	2014	CONCLUSIONS: In Asians, a combination test of UGT1A1*6 and UGT1A1*28 might be a potential biomarker of irinotecan-induced neutropenia, an observation that will need additional trials for confirmation.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
24308720-5	2014	CONCLUSIONS: In Asians, a combination test of UGT1A1*6 and UGT1A1*28 might be a potential biomarker of irinotecan-induced neutropenia, an observation that will need additional trials for confirmation.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
23888985-7	2014	Glucuronide capacity was present for the substrates 17beta-estradiol (estradiol-3-glucuronide, 2.9 +- 0.2 nmol/mg protein/min) and 4-methylumbelliferone (31.3 +- 3.3 nmol/mg protein/min), assuming that cats have functional homologue enzymes to at least the human UGT1A1 and probably other UGT1A isozymes.	Glucuronides	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	263-269
24439671-0	2014	Regulation and expression of aberrant methylation on irinotecan metabolic genes CES2, UGT1A1 and GUSB in the in-vitro cultured colorectal cancer cells.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
24439671-8	2014	CONCLUSION: Methylation in UGT1A1 gene expression silencing as an important mechanism; methylation could provide an effective target for methylation regulation intervening in the treatment of CPT-11.	Irinotecan	192-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
24243081-5	2014	Application of our model revealed that an absolute value or a steady state increase in bilirubin falling below 3.8Phi micromol/L (where Phi is a correction factor, =1 for UGT1A1 wild type and  1 for UGT1A1 variants) could be used to predict suboptimal atazanavir exposure and treatment failure.	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
24243081-5	2014	Application of our model revealed that an absolute value or a steady state increase in bilirubin falling below 3.8Phi micromol/L (where Phi is a correction factor, =1 for UGT1A1 wild type and  1 for UGT1A1 variants) could be used to predict suboptimal atazanavir exposure and treatment failure.	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
24243081-5	2014	Application of our model revealed that an absolute value or a steady state increase in bilirubin falling below 3.8Phi micromol/L (where Phi is a correction factor, =1 for UGT1A1 wild type and  1 for UGT1A1 variants) could be used to predict suboptimal atazanavir exposure and treatment failure.	Atazanavir Sulfate	252-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
24243081-5	2014	Application of our model revealed that an absolute value or a steady state increase in bilirubin falling below 3.8Phi micromol/L (where Phi is a correction factor, =1 for UGT1A1 wild type and  1 for UGT1A1 variants) could be used to predict suboptimal atazanavir exposure and treatment failure.	Atazanavir Sulfate	252-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
24243081-6	2014	Thus, we have successfully established a new mathematical approach for pharmacodynamic-pharmacokinetic modelling of the interaction between atazanavir and bilirubin, as it relates to genetic variants of UGT1A1.	Atazanavir Sulfate	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-209
24243081-6	2014	Thus, we have successfully established a new mathematical approach for pharmacodynamic-pharmacokinetic modelling of the interaction between atazanavir and bilirubin, as it relates to genetic variants of UGT1A1.	Bilirubin	155-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-209
23888985-7	2014	Glucuronide capacity was present for the substrates 17beta-estradiol (estradiol-3-glucuronide, 2.9 +- 0.2 nmol/mg protein/min) and 4-methylumbelliferone (31.3 +- 3.3 nmol/mg protein/min), assuming that cats have functional homologue enzymes to at least the human UGT1A1 and probably other UGT1A isozymes.	Estradiol	52-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	263-269
23888985-7	2014	Glucuronide capacity was present for the substrates 17beta-estradiol (estradiol-3-glucuronide, 2.9 +- 0.2 nmol/mg protein/min) and 4-methylumbelliferone (31.3 +- 3.3 nmol/mg protein/min), assuming that cats have functional homologue enzymes to at least the human UGT1A1 and probably other UGT1A isozymes.	estradiol-3-glucuronide	70-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	263-269
23888985-7	2014	Glucuronide capacity was present for the substrates 17beta-estradiol (estradiol-3-glucuronide, 2.9 +- 0.2 nmol/mg protein/min) and 4-methylumbelliferone (31.3 +- 3.3 nmol/mg protein/min), assuming that cats have functional homologue enzymes to at least the human UGT1A1 and probably other UGT1A isozymes.	Hymecromone	131-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	263-269
24815493-0	2014	Clinical observations on associations between the UGT1A1 genotype and severe toxicity of irinotecan.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
24815493-2	2014	UDP glucuronosyltransferase1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38 but the relationship between UGT1A1 and severe toxicity remains unclear.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
24815493-2	2014	UDP glucuronosyltransferase1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38 but the relationship between UGT1A1 and severe toxicity remains unclear.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
24815493-2	2014	UDP glucuronosyltransferase1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38 but the relationship between UGT1A1 and severe toxicity remains unclear.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
24815493-10	2014	CONCLUSIONS: Our study support the conclusion that patients with a UGT1A1*28 allele (s) will suffer an increased risk of severe irinotecan-induced diarrhea, whether with mid-or low-dosage.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
24815493-12	2014	Higher serum total bilirubin is an indication that patients UGT1A1 genotype is not wild-type, with significance for clinic usage of CPT-11.	Bilirubin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
24815493-12	2014	Higher serum total bilirubin is an indication that patients UGT1A1 genotype is not wild-type, with significance for clinic usage of CPT-11.	Irinotecan	132-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
25967674-0	2014	Prevalence of the UGT1A1*6 (c.211G&gt;A) Polymorphism and Prediction of Irinotecan Toxicity in Iranian Populations of Different Ethnicities.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
25967674-1	2014	BACKGROUND: Pharmacogenetic studies on irinotecan treatment in patients with metastatic colorectal cancer have indicated that genetic polymorphisms in UGT1A1*6 can lead to decreased enzyme activity and accumulation of the toxic metabolite SN-38.	Irinotecan	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
25967674-1	2014	BACKGROUND: Pharmacogenetic studies on irinotecan treatment in patients with metastatic colorectal cancer have indicated that genetic polymorphisms in UGT1A1*6 can lead to decreased enzyme activity and accumulation of the toxic metabolite SN-38.	Irinotecan	239-244	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
25967674-9	2014	CONCLUSION: The identification of the UGT1A1*6 alleles is necessary among the different Iranian ethnic groups before irinotecan therapy, suggesting that genotyping would be helpful for clinicians to optimize chemotherapy or identify individuals at risk of adverse drug reactions before clinical trials.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
24104197-4	2014	The polymorphisms evaluated included those in genes encoding putative acetaminophen-metabolizing enzymes (UGT1A1, UGT1A6, UGT1A9, UGT2B15, SULT1A1, CYP2E1, and CYP3A5) as well as CD44 and BHMT1.	Acetaminophen	70-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
25016708-1	2014	BACKGROUND: Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is a key conjugating enzyme of bilirubin and the anti-tumor medication irinotecan.	Bilirubin	101-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-60
25016708-1	2014	BACKGROUND: Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is a key conjugating enzyme of bilirubin and the anti-tumor medication irinotecan.	Bilirubin	101-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25016708-1	2014	BACKGROUND: Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is a key conjugating enzyme of bilirubin and the anti-tumor medication irinotecan.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-60
25016708-1	2014	BACKGROUND: Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is a key conjugating enzyme of bilirubin and the anti-tumor medication irinotecan.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25016708-2	2014	Comprehensive analysis of UGT1A1 gene polymorphisms may provide benefit by predicting pharmacokinetics and outcomes of treatment with irinotecan and certain antiviral medications.	Irinotecan	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
23965644-6	2014	We demonstrate that UGT1A1 and UGT1A3 are mainly responsible for pterostilbene glucuronidation although UGT1A8, UGT1A9 and UGT1A10 also had detectable activity.	pterostilbene	65-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23965644-7	2014	Intriguingly, UGT1A1 exhibits the highest activity against both resveratrol and pterostilbene despite altered hydroxyl group specificity.	Resveratrol	64-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
23965644-7	2014	Intriguingly, UGT1A1 exhibits the highest activity against both resveratrol and pterostilbene despite altered hydroxyl group specificity.	pterostilbene	80-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
24055854-6	2014	17beta-Estradiol was used as the marker substrate to determine UGT1A1 activities.	Estradiol	0-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
23965644-7	2014	Intriguingly, UGT1A1 exhibits the highest activity against both resveratrol and pterostilbene despite altered hydroxyl group specificity.	Hydroxyl Radical	110-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
24025985-6	2014	UGT1A1, -1A6, -1A7, -1A8, -1A9 and -1A10 participated in the formation of 7-O-G, while the formation of 8-O-G was catalyzed selectively by UGT1A6 and UGT1A9.	7-o-g	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24898899-0	2014	Influence of UGT1A1 6, 27, and 28 polymorphisms on nilotinib-induced hyperbilirubinemia in Japanese patients with chronic myeloid leukemia.	nilotinib	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
24898899-1	2014	Nilotinib potently inhibits human uridine diphosphate-glucuronosyltransferase (UGT1A1) activity, causing hyperbilirubinemia.	nilotinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
24898899-4	2014	The median time to elevation of bilirubin levels in UGT1A1 poor metabolizers was 2.0 weeks (hazard ratio, 6.11).	Bilirubin	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
24898899-5	2014	The median time to reduction in nilotinib dose in UGT1A1 poor metabolizers was 4.0 weeks (hazard ratio, 7.52; p = 0.002).	nilotinib	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
24898899-6	2014	Consequently, in the maintenance phase 3 months following the initiation of nilotinib therapy, the median daily dose and C0 of nilotinib were 350 mg/day and 372 ng/mL, respectively, in UGT1A1 poor metabolizers, and 600 mg/day and 804 ng/mL, respectively, in the other patients.	nilotinib	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
24295085-7	2014	Substrates, inhibitors or inducers of UGT1A1 and CYP3A may also affect the pharmacokinetic profile of indacaterol.	indacaterol	102-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
24256624-7	2014	Propofol (UGT1A9 inhibitor) effectively blocked G4 generation in HLMs (IC50 63.7 +- 11.6 microM), whereas the UGT1A1 inhibitor bilirubin only produced partial inhibition in HLMs and HIMs.	Bilirubin	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
24096683-1	2014	PURPOSE: Dolutegravir (DTG), an unboosted HIV integrase inhibitor (INI), is metabolized by UGT1A1 and to a minor extent by CYP3A.	dolutegravir	9-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
24096683-1	2014	PURPOSE: Dolutegravir (DTG), an unboosted HIV integrase inhibitor (INI), is metabolized by UGT1A1 and to a minor extent by CYP3A.	dolutegravir	23-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
24642571-0	2014	FOLFIRI combined with bevacizumab as first-line treatment for metastatic colorectal cancer patients with hyperbilirubinemia after UGT1A1 genotyping.	FOLFIRI regimen	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
24642571-1	2014	OBJECTIVE: To report a metastatic colorectal cancer patient with hyperbilirubinemia treated with a combination of bevacizumab and FOLFIRI (5-fluorouracil, leucovorin, and irinotecan) using uridine diphosphate glucuronosyl transferase (UGT1A1) genotyping.	FOLFIRI regimen	130-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	235-241
24195503-11	2014	Analysis of UGT1A1 alleles may be the basis for modified dosing and reducing the potential toxicity of irinotecan.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
24523126-13	2014	Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh.	Bilirubin	126-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
24523126-13	2014	Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh.	Bilirubin	208-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-104
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-111
24329186-0	2014	Evaluation of the effect of UGT1A1 polymorphisms on dolutegravir pharmacokinetics.	dolutegravir	52-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
24195516-11	2014	The promoter of the UGT1A1 gene in colorectal cancer cells is methylated, which is an important mechanism of UGT1A1 gene silencing and can be regarded as the target point of research for CPT-11 drug resistance and control mechanisms for the reversal of drug resistance.	Irinotecan	187-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
24329186-1	2014	AIM: To evaluate potential pharmacogenetic effects of UGT1A1 polymorphisms on the pharmacokinetics (PK) of dolutegravir (Tivicay ; ViiV Healthcare, NC, USA), an HIV-1 integrase inhibitor.	dolutegravir	107-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
24601226-6	2014	At 100 microM of bakuchiol, the activity of UGT1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9 and 1A10 was inhibited by -46.2%, 74.7%, 17.8%, 98.7%, 70.4%, 99.2%, 75.8%, and 93.3%, respectively.	bakuchiol	17-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
24329186-4	2014	CONCLUSION: Increased dolutegravir exposure in carriers of UGT1A1 reduced function polymorphisms is not clinically significant based on accumulated safety data so dose adjustment in these individuals is not required.	dolutegravir	22-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
24063841-1	2013	Whether conjugated bilirubin concentration, resulting from hepatic UDP-glucuronosyltransferase 1 A1 activity, is associated with cardiovascular disease is unknown.	Bilirubin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-99
25147562-4	2014	Human hepatocytes (HH) and HepG2 cells sustained similar treatments, except that the expression of the bilirubin conjugating UDP-glucuronosyltransferase (UGT) 1A1 enzyme and multidrug resistance-associated protein (MRP) 2 transporter was analyzed.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-162
24217933-0	2014	Role of UGT1A1 and ADH gene polymorphisms in pegvisomant-induced liver toxicity in acromegalic patients.	pegvisomant	45-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
24088669-0	2013	Polymorphisms in the UGT1A1 gene predict adverse effects of irinotecan in the treatment of gynecologic cancer in Japanese patients.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
24349450-7	2013	We also found that BPAF glucuronidation could be mediated through several human recombinant UDP-glucuronosyltransferases (UGTs) including UGT1A1, UGT1A3, UGT1A8, UGT1A9, UGT2B4, UGT2B7, UGT2B15 and UGT2B17, among which UGT2B7 showed the highest efficiency of glucuronidation.	4,4'-hexafluorisopropylidene diphenol	19-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
24033692-0	2013	UGT1A1*6, 1A7*3, and 1A9*22 genotypes predict severe neutropenia in FOLFIRI-treated metastatic colorectal cancer in two prospective studies in Japan.	FOLFIRI regimen	68-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24033692-1	2013	UNLABELLED: Retrospective studies have suggested that UDP-glucuronosyltransferase (UGT)1A1, UGT1A7, and UGT1A9 predict severe toxicity and efficacy of irinotecan-containing regimens.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-90
24114122-0	2013	UGT1A1 genotype-guided phase I study of irinotecan, oxaliplatin, and capecitabine.	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24114122-0	2013	UGT1A1 genotype-guided phase I study of irinotecan, oxaliplatin, and capecitabine.	Oxaliplatin	52-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24114122-0	2013	UGT1A1 genotype-guided phase I study of irinotecan, oxaliplatin, and capecitabine.	Capecitabine	69-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24114122-11	2013	UGT1A1 *1/*28 and *1/*1 patients treated with IRIN (150) had similar AUCs for the active irinotecan metabolite, SN38 (366 +/- 278 and 350 +/- 159 ng/ml*hr, respectively).	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24114122-14	2013	CONCLUSIONS: UGT1A1 genotype affects the dose and pharmacokinetics of the CAPIRINOX regimen and UGT1A1 genotype-guided dosing of CAPIRINOX is ongoing in a phase II study of small bowel cancer (NCT00433550).	capirinox	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
24114122-14	2013	CONCLUSIONS: UGT1A1 genotype affects the dose and pharmacokinetics of the CAPIRINOX regimen and UGT1A1 genotype-guided dosing of CAPIRINOX is ongoing in a phase II study of small bowel cancer (NCT00433550).	capirinox	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
24088669-6	2013	Homozygosity for UGT1A1*6/*6 and heterozygosity for UGT1A1*6/*28 were associated with an increased risk of absolute neutrophil count and/or diarrhea in Japanese gynecologic cancer patients, despite the lower doses of irinotecan used in these patients.	Irinotecan	217-227	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
24088669-7	2013	UGT1A1*6 and UGT1A1*28 are potential predictors of severe absolute neutrophil decrease and diarrhea caused by low-dose irinotecan in gynecologic cancer patients.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24088669-1	2013	Irinotecan is a key chemotherapeutic drug used to treat many tumors, including cervical and ovarian cancers; however, irinotecan can cause toxicity, particularly in the presence of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphisms, which are associated with reduced enzyme activity.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
24088669-7	2013	UGT1A1*6 and UGT1A1*28 are potential predictors of severe absolute neutrophil decrease and diarrhea caused by low-dose irinotecan in gynecologic cancer patients.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
24088669-1	2013	Irinotecan is a key chemotherapeutic drug used to treat many tumors, including cervical and ovarian cancers; however, irinotecan can cause toxicity, particularly in the presence of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphisms, which are associated with reduced enzyme activity.	Irinotecan	118-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
24088669-2	2013	Here, we investigated the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28) and their relationships with irinotecan-induced adverse events in patients with gynecologic cancer, who are treated with lower doses of irinotecan than patients with other types of solid tumors.	Irinotecan	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
24088669-2	2013	Here, we investigated the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28) and their relationships with irinotecan-induced adverse events in patients with gynecologic cancer, who are treated with lower doses of irinotecan than patients with other types of solid tumors.	Irinotecan	247-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
24057187-1	2013	Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is an important metabolic process during which steroids are converted to more easily excreted compounds in steroid target tissues, such as the prostate.	Steroids	129-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-64
24057187-1	2013	Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is an important metabolic process during which steroids are converted to more easily excreted compounds in steroid target tissues, such as the prostate.	Steroids	129-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
24057187-1	2013	Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is an important metabolic process during which steroids are converted to more easily excreted compounds in steroid target tissues, such as the prostate.	Steroids	129-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-64
24057187-1	2013	Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is an important metabolic process during which steroids are converted to more easily excreted compounds in steroid target tissues, such as the prostate.	Steroids	129-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
24107802-0	2013	Hyperbilirubinemia in pazopanib- or sunitinib-treated patients in COMPARZ is associated with UGT1A1 polymorphisms.	pazopanib	22-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24244442-0	2013	UDP-glucuronosyltransferase 1A compromises intracellular accumulation and anti-cancer effect of tanshinone IIA in human colon cancer cells.	tanshinone	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
24129235-8	2013	The SU11274 significantly decreased the expression of UGT1A1, but not ABCG2 and ABCB1.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	4-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
24107802-0	2013	Hyperbilirubinemia in pazopanib- or sunitinib-treated patients in COMPARZ is associated with UGT1A1 polymorphisms.	Sunitinib	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
23950218-1	2013	UDP-glucuronosyltransferase (UGT) 1A1 is the sole enzyme that can metabolize bilirubin.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23950218-7	2013	When HaCaT cells were treated with UVB-exposed tryptophan, UGT1A1 mRNA and activity were significantly induced.	Tryptophan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
23950218-8	2013	Treatment of the HaCaT cells with 6-formylindolo[3,2-b]carbazole, which is one of the tryptophan derivatives formed by UVB, resulted in an induction of UGT1A1 mRNA and activity.	6-formylindolo(3,2-b)carbazole	34-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
23950218-8	2013	Treatment of the HaCaT cells with 6-formylindolo[3,2-b]carbazole, which is one of the tryptophan derivatives formed by UVB, resulted in an induction of UGT1A1 mRNA and activity.	Tryptophan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
24204915-1	2013	Present study was aimed to explore the effect of (TA)n UGT1A1 gene promoter polymorphism on bilirubin metabolism, bilirubinaemia, predisposition to cholelithiasis and subsequent cholecystectomy, in Sickle-Cell Anemia (SCA) and beta-Thalasemia major (bTH) in Kuwaiti subjects compared to other population.	Bilirubin	92-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24104695-3	2013	Oleic acid, linoleic acid, and docosahexaenoic acid (DHA) strongly inhibited UGT1A1 activity.	Docosahexaenoic Acids	31-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
24047243-8	2013	UGT1A1 catalyzed the glucuronidation of B[a]P-7,8-catechol and generated two isomeric O-monoglucuronsyl-B[a]P-7,8-catechol products that were identified by RP-HPLC and by LC-MS/MS.	7,8-catechol	46-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24047243-8	2013	UGT1A1 catalyzed the glucuronidation of B[a]P-7,8-catechol and generated two isomeric O-monoglucuronsyl-B[a]P-7,8-catechol products that were identified by RP-HPLC and by LC-MS/MS.	o-monoglucuronsyl-b	86-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24047243-8	2013	UGT1A1 catalyzed the glucuronidation of B[a]P-7,8-catechol and generated two isomeric O-monoglucuronsyl-B[a]P-7,8-catechol products that were identified by RP-HPLC and by LC-MS/MS.	7,8-catechol	110-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24104695-0	2013	Impact of fatty acids on human UDP-glucuronosyltransferase 1A1 activity and its expression in neonatal hyperbilirubinemia.	Fatty Acids	10-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-62
24104695-3	2013	Oleic acid, linoleic acid, and docosahexaenoic acid (DHA) strongly inhibited UGT1A1 activity.	Docosahexaenoic Acids	53-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
24104695-2	2013	Here, the impact of fatty acids on human UDP-glucuronosyltransferase (UGT) 1A1--the sole enzyme that can metabolize bilirubin--were examined.	Fatty Acids	20-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-78
24104695-4	2013	Forty-eight hours after a treatment with a lower concentration of DHA (10 mg/kg), total bilirubin significantly increased in neonatal hUGT1 mice, which are human neonatal jaundice models.	Docosahexaenoic Acids	66-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-139
24104695-2	2013	Here, the impact of fatty acids on human UDP-glucuronosyltransferase (UGT) 1A1--the sole enzyme that can metabolize bilirubin--were examined.	Bilirubin	116-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-78
24104695-3	2013	Oleic acid, linoleic acid, and docosahexaenoic acid (DHA) strongly inhibited UGT1A1 activity.	Oleic Acid	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
24104695-4	2013	Forty-eight hours after a treatment with a lower concentration of DHA (10 mg/kg), total bilirubin significantly increased in neonatal hUGT1 mice, which are human neonatal jaundice models.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-139
24104695-5	2013	In contrast, treatments with higher concentrations of fatty acids (0.1-10 g/kg) resulted in a decrease in serum bilirubin in hUGT1 mice.	Fatty Acids	54-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-130
24104695-3	2013	Oleic acid, linoleic acid, and docosahexaenoic acid (DHA) strongly inhibited UGT1A1 activity.	Linoleic Acid	12-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
24104695-5	2013	In contrast, treatments with higher concentrations of fatty acids (0.1-10 g/kg) resulted in a decrease in serum bilirubin in hUGT1 mice.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-130
24104695-6	2013	It was further demonstrated that the treatment with higher concentrations of fatty acids induced UGT1A1, possibly by activation of peroxisome proliferator-activated receptors.	Fatty Acids	77-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
24104695-7	2013	Our data indicates that activation of peroxisome proliferator-activated receptors would increase UGT1A1 expression, resulting in reduction of serum bilirubin levels in human infants.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
23782005-11	2013	There was a significant association between UGT1A1 genotype and bilirubin grade in the maternal population (p=0.0006) but not neonates (p=0.49).	Bilirubin	64-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
23917319-6	2013	Glucuronide conjugates of rilpivirine and a monomethylhydroxylated metabolite of rilpivirine were also detected and were found to be formed by UDP-glucuronosyltransferases (UGTs) UGT1A4 and UGT1A1, respectively.	Glucuronides	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
23917319-6	2013	Glucuronide conjugates of rilpivirine and a monomethylhydroxylated metabolite of rilpivirine were also detected and were found to be formed by UDP-glucuronosyltransferases (UGTs) UGT1A4 and UGT1A1, respectively.	Rilpivirine	26-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
23917319-6	2013	Glucuronide conjugates of rilpivirine and a monomethylhydroxylated metabolite of rilpivirine were also detected and were found to be formed by UDP-glucuronosyltransferases (UGTs) UGT1A4 and UGT1A1, respectively.	Rilpivirine	81-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
23401472-1	2013	Human uridine 5"-diphospho-glucuronosyltransferase (UGT) 1A1 catalyzes the metabolism of numerous clinically and pharmacologically important compounds, such as bilirubin and SN-38.	Bilirubin	160-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-60
23401472-1	2013	Human uridine 5"-diphospho-glucuronosyltransferase (UGT) 1A1 catalyzes the metabolism of numerous clinically and pharmacologically important compounds, such as bilirubin and SN-38.	Irinotecan	174-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-60
23401472-4	2013	Bisulfite sequence analysis revealed that the CpG-rich region near the UGT1A1 promoter (-85 to +40) was hypermethylated (83%) in the kidney, whereas it was hypomethylated (37%) in the liver.	hydrogen sulfite	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
23401472-7	2013	Treatment with 5-aza-2"-deoxycytidine (5-aza-dC), an inhibitor of DNA methylation, resulted in an increase of UGT1A1 mRNA expression in both cell types, but the increase was much larger in HK-2 cells than in HuH-7 cells.	Decitabine	15-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
23401472-7	2013	Treatment with 5-aza-2"-deoxycytidine (5-aza-dC), an inhibitor of DNA methylation, resulted in an increase of UGT1A1 mRNA expression in both cell types, but the increase was much larger in HK-2 cells than in HuH-7 cells.	Decitabine	39-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
23401472-8	2013	The transfection of an HNF1alpha expression plasmid into the HK-2 cells resulted in an increase of UGT1A1 mRNA only in the presence of 5-aza-dC.	Decitabine	135-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
24522354-1	2013	BACKGROUND: In Europeans the TATA box TA7 repeat promoter variant in the UGT1A1 gene (UGT1A1*28) is the major determinant of bilirubin levels.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
23932761-3	2013	Nonetheless, recent Mendelian randomization analyses reveal that individuals who carry low expression alleles of the hepatic bilirubin conjugating enzyme UGT1A1, and hence have somewhat elevated levels of plasma bilirubin throughout life, are not at decreased risk for vascular disorders.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
23932761-3	2013	Nonetheless, recent Mendelian randomization analyses reveal that individuals who carry low expression alleles of the hepatic bilirubin conjugating enzyme UGT1A1, and hence have somewhat elevated levels of plasma bilirubin throughout life, are not at decreased risk for vascular disorders.	Bilirubin	212-221	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
24522354-1	2013	BACKGROUND: In Europeans the TATA box TA7 repeat promoter variant in the UGT1A1 gene (UGT1A1*28) is the major determinant of bilirubin levels.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
24065680-2	2013	These mutations result in the deficiency of UGT1A1, a hepatic enzyme essential for bilirubin conjugation.	Bilirubin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
24065680-4	2013	Molecular genetic analysis showed a homozygous UGT1A1 promoter mutation [A(TA)7TAA] and a heterozygous insertion of 1 adenosine nucleotide between positions 353 and 354 in exon 1 of UGT1A1 that caused a frameshift with a premature stop codon.	adenosine nucleotide	118-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
23750830-16	2013	These data suggest that the proposed surrogate probe substrates to evaluate the in vitro inhibition of UGT1A1, OATP1B1, and BSEP may be suitable to assess bilirubin disposition.	Bilirubin	155-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
23726867-6	2013	Up-regulation of metabolic enzyme genes provided evidence for the involvement of phase I (CYP1A1, CYP1B1, ALDH1A2 and CES2) and phase II (UGT1A6, UGT1A1, NAT1 and GSTM3) enzymes in the detoxification response and potential activation of CYN.	cylindrospermopsin	237-240	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
23677771-10	2013	Axitinib is metabolized primarily in the liver by cytochrome P450 (CYP) 3A4/5 and, to a lesser extent (&lt;10 % each), by CYP1A2, CYP2C19, and uridine diphosphate glucuronosyltransferase (UGT) 1A1.	Axitinib	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-196
23892411-0	2013	Analysis of UGT1A1*28 genotype and SN-38 pharmacokinetics for irinotecan-based chemotherapy in patients with advanced colorectal cancer: results from a multicenter, retrospective study in Shanghai.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23892411-1	2013	BACKGROUND: The UGT1A1*28 polymorphism, although closely linked with CPT-11-related adverse effects, cannot be used alone to guide individualized treatment decisions.	Irinotecan	69-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
23892411-6	2013	To understand differences in genotype expression, the frequency of UGT1A1*28 thymine-adenine (TA) repeats in TATA box arrangement was assessed by PCR with genomic DNA extracted from peripheral blood.	thymine-adenine	77-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
23892411-6	2013	To understand differences in genotype expression, the frequency of UGT1A1*28 thymine-adenine (TA) repeats in TATA box arrangement was assessed by PCR with genomic DNA extracted from peripheral blood.	Tantalum	94-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
24147345-2	2013	in vitro incubation method using recombinant UGTs-catalyzed 4-methylumbelliferone (4-MU) glucuronidation was used to evaluate the inhibition towards important UGT isoforms in the liver, including UGT1A1, 1A3, 1A6, 1A9, and 2B7.	Hymecromone	83-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
23786524-0	2013	Mutual regioselective inhibition of human UGT1A1-mediated glucuronidation of four flavonoids.	Flavonoids	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
23669385-8	2013	An inactive ether glucuronide, formed primarily via UGT1A1, was the principal biotransformation product at 18.9% of the dose excreted in urine and the principal metabolite in plasma.	ether glucuronide	12-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
23786524-1	2013	UDP-glucuronosyltransferase (UGT) 1A1-catalyzed glucuronidation is an important elimination pathway of flavonoids, and mutually inhibitory interactions may occur when two or more flavonoids are coadministered.	Flavonoids	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23786524-1	2013	UDP-glucuronosyltransferase (UGT) 1A1-catalyzed glucuronidation is an important elimination pathway of flavonoids, and mutually inhibitory interactions may occur when two or more flavonoids are coadministered.	Flavonoids	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23786524-2	2013	Our recent research suggested that glucuronidation of flavonoids displayed distinct positional preferences, but whether this will lead to the mutually regioselective inhibition of UGT1A1-mediated glucuronidation of flavonoids is unknown.	Flavonoids	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
23786524-2	2013	Our recent research suggested that glucuronidation of flavonoids displayed distinct positional preferences, but whether this will lead to the mutually regioselective inhibition of UGT1A1-mediated glucuronidation of flavonoids is unknown.	Flavonoids	215-225	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
23689708-1	2013	Atazanavir (ATV) causes an elevation of unconjugated hyperbilirubinemia (HBR) as a result of UDP glucuronyltransferase (UGT) 1A1 inhibition.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-128
23898114-0	2013	UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism-directed phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23898114-0	2013	UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism-directed phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer.	doxifluridine	97-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23689708-1	2013	Atazanavir (ATV) causes an elevation of unconjugated hyperbilirubinemia (HBR) as a result of UDP glucuronyltransferase (UGT) 1A1 inhibition.	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-128
23898114-0	2013	UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism-directed phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer.	doxifluridine	123-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23898114-1	2013	AIM: We performed a phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer based on UDP-glucuronosyltransferase (UGT) 1A1 polymorphism.	Irinotecan	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-168
23800356-0	2013	Recurrent cervical cancer in a patient who was compound heterozygous for UGT1A1*6 and UGT1A1*28 presenting with serious adverse events during irinotecan hydrochloride/nedaplatin therapy.	Irinotecan	142-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
23898114-1	2013	AIM: We performed a phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer based on UDP-glucuronosyltransferase (UGT) 1A1 polymorphism.	doxifluridine	54-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-168
23898114-1	2013	AIM: We performed a phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer based on UDP-glucuronosyltransferase (UGT) 1A1 polymorphism.	doxifluridine	80-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-168
23800356-0	2013	Recurrent cervical cancer in a patient who was compound heterozygous for UGT1A1*6 and UGT1A1*28 presenting with serious adverse events during irinotecan hydrochloride/nedaplatin therapy.	Irinotecan	142-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	Irinotecan	43-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	211-217
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	Irinotecan	43-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	224-230
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	Irinotecan	162-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	211-217
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	nedaplatin	173-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	211-217
23926009-1	2013	OBJECTIVE: To analyze potential mutations of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene in patients with unconjugated hyperbilirubinemia, and to explore the correlation between the mutations and total serum bilirubin levels.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-92
23580084-0	2013	UGT1A1*28 is associated with decreased systemic exposure of atorvastatin lactone.	Atorvastatin lactone	60-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23580084-2	2013	Atorvastatin acid is converted to its corresponding lactone form spontaneously or via glucuronidation mediated by uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A3.	Atorvastatin	0-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-175
23580084-2	2013	Atorvastatin acid is converted to its corresponding lactone form spontaneously or via glucuronidation mediated by uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A3.	Lactones	52-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-175
23580084-8	2013	RESULTS: Carriers of the low-expression allele UGT1A1*28(TA) 7 tended to have lower levels of atorvastatin lactone (p &lt; 0.05) than carriers with the normal-activity allele (TA) 6 .	Atorvastatin lactone	94-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
23580084-9	2013	CONCLUSION: The low-expression UGT1A1*28(TA) 7 allele seems to be associated with decreased systemic exposure of the suspected muscle-toxic metabolite atorvastatin lactone.	Atorvastatin lactone	151-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
23065713-4	2013	Data fitting using Dixon and Lineweaver-Burk plots demonstrated the competitive inhibition of liquiritigenin towards UGT1A1 and UGT1A9-mediated 4-MU glucuronidation reaction.	liquiritigenin	94-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
23926009-1	2013	OBJECTIVE: To analyze potential mutations of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene in patients with unconjugated hyperbilirubinemia, and to explore the correlation between the mutations and total serum bilirubin levels.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
23926009-8	2013	CONCLUSION: The level of total serum bilirubin is correlated with the number of UGT1A1 gene mutations as well as their heterozygous or homozygous status.	Bilirubin	37-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
23606168-5	2013	BCL11A and XmnI polymorphisms had significant effects on baseline HbF, while UGT1A1 promoter polymorphisms significantly influenced baseline serum bilirubin.	Bilirubin	147-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
23753274-4	2013	Second, taking advantage of mendelian randomization, we tested whether a genetic variant in the bilirubin glucoronidating enzyme UGT1A1 (rs6742078) was associated with increased plasma bilirubin levels and, in turn, with an increased risk of symptomatic gallstone disease.	Bilirubin	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
23753274-4	2013	Second, taking advantage of mendelian randomization, we tested whether a genetic variant in the bilirubin glucoronidating enzyme UGT1A1 (rs6742078) was associated with increased plasma bilirubin levels and, in turn, with an increased risk of symptomatic gallstone disease.	Bilirubin	185-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
23753274-8	2013	UGT1A1 genotype explained 20% of the total variation in plasma bilirubin levels and was associated with increases in the mean plasma bilirubin level overall of +16% (+0.09 mg/dL) in GT heterozygotes and +90% (+0.50 mg/dL) in TT homozygotes compared with GG homozygotes, with similar effects in women and men (P for trend &lt;.001 for all).	Bilirubin	63-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23753274-8	2013	UGT1A1 genotype explained 20% of the total variation in plasma bilirubin levels and was associated with increases in the mean plasma bilirubin level overall of +16% (+0.09 mg/dL) in GT heterozygotes and +90% (+0.50 mg/dL) in TT homozygotes compared with GG homozygotes, with similar effects in women and men (P for trend &lt;.001 for all).	Bilirubin	133-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	108-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
24060717-0	2013	UGT1A1 promoter polymorphism associated with serum bilirubin level in Saudi patients with sickle cell disease.	Bilirubin	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24060717-1	2013	BACKGROUND AND OBJECTIVES: Polymorphism in (TA)n of the UGT1A1 promoter influences bilirubin level and risk of gallstones in patients with sickle cell disease (SCD) of African descent.	Bilirubin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
24060717-8	2013	Increased (TA)n of the UGT1A1 promoter (P &lt; .0001), male gender (P=.02), higher LDH (P=.001), and lower Hb level (P=.009) were associated with higher bilirubin level, while the co-inheritance of a-thalassemia (P=.003) was linked with lower bilirubin level.	Bilirubin	153-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
24060717-8	2013	Increased (TA)n of the UGT1A1 promoter (P &lt; .0001), male gender (P=.02), higher LDH (P=.001), and lower Hb level (P=.009) were associated with higher bilirubin level, while the co-inheritance of a-thalassemia (P=.003) was linked with lower bilirubin level.	Bilirubin	243-252	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
24060717-12	2013	CONCLUSION: (TA)n in the UGT1A1 promoter and intensity of hemolysis modify steady-state serum bilirubin level in SCD.	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
23682072-4	2013	Using homogenates from HEK293 UGT-overexpressing cell lines, raloxifene was shown to be glucuronidated primarily by the hepatic UGTs 1A1 and 1A9 and the extra-hepatic UGTs 1A8 and 1A10; no detectable raloxifene glucuronidation activity was found for UGT2B enzymes.	Raloxifene Hydrochloride	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-144
23682072-5	2013	Functional UGT1A1 transcriptional promoter genotypes were significantly (Ptrend = 0.005) associated with ral-6-Gluc formation in human liver microsomes, and, consistent with the decreased raloxifene glucuronidation activities observed in vitro with cell lines overexpressing UGT1A8 variants, the UGT1A8*2 variant was significantly (P = 0.023) correlated with total raloxifene glucuronide formation in human jejunum homogenates.	Raloxifene Hydrochloride	188-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
23682072-5	2013	Functional UGT1A1 transcriptional promoter genotypes were significantly (Ptrend = 0.005) associated with ral-6-Gluc formation in human liver microsomes, and, consistent with the decreased raloxifene glucuronidation activities observed in vitro with cell lines overexpressing UGT1A8 variants, the UGT1A8*2 variant was significantly (P = 0.023) correlated with total raloxifene glucuronide formation in human jejunum homogenates.	Raloxifene Hydrochloride	365-375	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
23682072-5	2013	Functional UGT1A1 transcriptional promoter genotypes were significantly (Ptrend = 0.005) associated with ral-6-Gluc formation in human liver microsomes, and, consistent with the decreased raloxifene glucuronidation activities observed in vitro with cell lines overexpressing UGT1A8 variants, the UGT1A8*2 variant was significantly (P = 0.023) correlated with total raloxifene glucuronide formation in human jejunum homogenates.	Glucuronides	376-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	Glucuronides	116-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	129-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	Sulfates	143-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	129-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
23595344-10	2013	CONCLUSION: Irinotecan dosing based on UGT1A1*28 and *6 is feasible, and higher doses of irinotecan can be safely administered in patients with 0 or 1 DA, compared to those with 2 DA.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23713759-6	2013	Moreover, the A-ring OH-4 group promoted glucuronidation at the 2" position for the reaction of 4,2"-dihydroxychalcone with UGT1A1 and 1A3.	4,2'-DIHYDROXYCHALCONE	96-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-138
23840132-0	2013	Severe irinotecan-induced toxicity in a patient with UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
23840132-0	2013	Severe irinotecan-induced toxicity in a patient with UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
23840132-1	2013	Many studies have demonstrated the impact of UGT1A1 on toxicity of irinotecan.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
23840132-3	2013	Based on this, prescribers of irinotecan are advised that patients with UGT1A1 28 (TA 7/7) should start with a reduced dose of irinotecan, although a particular dose is not specified.	Irinotecan	30-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
23840132-3	2013	Based on this, prescribers of irinotecan are advised that patients with UGT1A1 28 (TA 7/7) should start with a reduced dose of irinotecan, although a particular dose is not specified.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
23840132-4	2013	Research in Asian countries has shown a lower incidence of UGT1A1 28 (TA 7/7), while UGT1A1 6 (A/A) is more often found and is associated with severe irinotecan-related neutropenia.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
23840132-8	2013	Additional studies will be necessary to determine the optimal starting dose of irinotecan for patients with both UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
23840132-8	2013	Additional studies will be necessary to determine the optimal starting dose of irinotecan for patients with both UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
23595344-0	2013	A UGT1A1*28 and *6 genotype-directed phase I dose-escalation trial of irinotecan with fixed-dose capecitabine in Korean patients with metastatic colorectal cancer.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	2-8
23595344-0	2013	A UGT1A1*28 and *6 genotype-directed phase I dose-escalation trial of irinotecan with fixed-dose capecitabine in Korean patients with metastatic colorectal cancer.	Capecitabine	97-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	2-8
23595344-1	2013	PURPOSE: UGT1A1 genotypes are important when considering treatment with irinotecan-containing regimens.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
23595344-2	2013	In this study, we determined the dose, efficacy, and tolerability of irinotecan according to UGT1A1 genotypes when combined with capecitabine in patients with metastatic colorectal cancer.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
23559402-9	2013	Polymorphisms in CYP2C9, TPMT, UGT1A1, MDR1, and 5-HTR2A were related to some adverse effects of olanzapine.	Olanzapine	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
23241680-0	2013	Microarray with LNA-probes for genotyping of polymorphic variants of Gilbert"s syndrome gene UGT1A1(TA)n. BACKGROUND: Gilbert"s syndrome is a common metabolic dysfunction characterized by elevated levels of unconjugated bilirubin in the bloodstream.	Bilirubin	220-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
23537215-0	2013	The association between heterozygosity for UGT1A1*6, UGT1A1*28, and variation in the serum total-bilirubin level in healthy young Japanese adults.	Bilirubin	97-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
23537215-10	2013	Multiple regression analysis showed significant relationships between the serum total-bilirubin level, the UGT1A1 genotypes *1/*28 and *6/*28, and sex.	Bilirubin	86-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
23537215-12	2013	CONCLUSIONS: We found that the UGT1A1 genotypes *1/*28 and *6/*28 as well as sex contributed to interindividual variations in the serum total-bilirubin levels.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
23537215-13	2013	In contrast, UGT1A1*1/*6 showed only minimal involvement in individual differences in serum total-bilirubin levels.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
23647681-1	2013	OBJECTIVES: Interindividual variability in glucuronidation of bilirubin and drugs by UDP-glucuronosyltransferase 1A1 (UGT1A1) is considerable and only partially explained by genetic polymorphisms and enzyme inducers.	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-116
23647681-1	2013	OBJECTIVES: Interindividual variability in glucuronidation of bilirubin and drugs by UDP-glucuronosyltransferase 1A1 (UGT1A1) is considerable and only partially explained by genetic polymorphisms and enzyme inducers.	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
23647681-6	2013	Multivariate regression analysis identified *28/*28 genotype, -4 CpG site methylation and alcohol history as significant predictors of UGT1A1 protein content.	Alcohols	90-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
23647681-7	2013	Exclusion of livers with *28/*28 genotype or alcohol history revealed positive correlations of -4 CpG methylation with bilirubin glucuronidation (R = 0.73, P &lt; 0.00001) and UGT1A1 protein content (R = 0.54, P = 0.008).	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
23737969-10	2013	Body weight &gt;=40 kg and homozygosity for UGT1A1*6 were risk factors of creatinine elevation (OR = 8.48, 95% CI = 1.7-43.57, P = 0.010 and OR = 14.17, 95% CI = 1.34-150.35, P = 0.028).	Creatinine	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
23387445-0	2013	Phase I and II metabolism and MRP2-mediated export of bosentan in a MDCKII-OATP1B1-CYP3A4-UGT1A1-MRP2 quadruple-transfected cell line.	Bosentan	54-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
23387445-8	2013	Additionally, a direct glucuronide of bosentan could be identified intracellularly in cell lines expressing UGT1A1 and in the apical compartments of cell lines expressing UGT1A1 and MRP2.	Glucuronides	23-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
23387445-8	2013	Additionally, a direct glucuronide of bosentan could be identified intracellularly in cell lines expressing UGT1A1 and in the apical compartments of cell lines expressing UGT1A1 and MRP2.	Glucuronides	23-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
23387445-8	2013	Additionally, a direct glucuronide of bosentan could be identified intracellularly in cell lines expressing UGT1A1 and in the apical compartments of cell lines expressing UGT1A1 and MRP2.	Bosentan	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
23387445-8	2013	Additionally, a direct glucuronide of bosentan could be identified intracellularly in cell lines expressing UGT1A1 and in the apical compartments of cell lines expressing UGT1A1 and MRP2.	Bosentan	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
23387445-9	2013	CONCLUSIONS AND IMPLICATIONS: These in vitro data indicate that bosentan is a substrate of UGT1A1.	Bosentan	64-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
23090703-2	2013	This study was performed to examine whether common polymorphisms in UGT1A1, UGT2B7, CYP2C19 and ABCB1 affect the PK of labetalol.	Labetalol	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
23408116-7	2013	Cotransfection studies demonstrated an inhibitory effect of exon 5b containing cDNAs on acetaminophen glucuronidation by UGT1A1 and UGT1A6 cDNAs containing exon 5a.	exon 5b	60-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
23408116-7	2013	Cotransfection studies demonstrated an inhibitory effect of exon 5b containing cDNAs on acetaminophen glucuronidation by UGT1A1 and UGT1A6 cDNAs containing exon 5a.	Acetaminophen	88-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
23299247-6	2013	Demethylation was inhibited significantly by furafylline and predominantly catalysed by recombinant CYP1A2, whereas glucuronidation was inhibited by silibinin, quercetin, as well as 1-naphthol and catalysed by recombinant UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9 and UGT1A10.	1-naphthol	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
23888707-3	2013	Additionally, effects of PA and PC on UGT1A1 mRNA and protein expressions were also measured after transient transfection of a specific CAR siRNA for 72 h in HepG2 cells.	praeruptorin C	32-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
23888707-5	2013	The results suggest that PA and PC can significantly up-regulate UGT1A1 expression partially via the CAR-mediated pathway.	praeruptorin A	25-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
23888707-5	2013	The results suggest that PA and PC can significantly up-regulate UGT1A1 expression partially via the CAR-mediated pathway.	praeruptorin C	32-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
23619273-3	2013	We analyzed the polymorphism A(TA)&lt;formula&gt;_{n}&lt;/formula&gt; TAA at the UGT1A1 promoter and the relationships between the various A(TA)&lt;formula&gt;_{n}&lt;/formula&gt; TAA genotypes and alleles and bilirubin levels and occurrence of cholelithiasis.	Bilirubin	210-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
23548653-0	2013	Effect of the UGT1A1*28 allele on unconjugated hyperbilirubinemia in HIV-positive patients receiving Atazanavir: a systematic review.	Atazanavir Sulfate	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
23548653-1	2013	OBJECTIVE: To systematically examine the literature assessing the effect of uridine 5"-diphospho-glucuronosyltransferase (UGT)1A1*28 genetic polymorphisms on atazanavir-associated hyperbilirubinemia.	Atazanavir Sulfate	158-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
23090703-10	2013	Future larger studies are needed to evaluate the effect of CYP2C19 and UGT1A1 polymorphisms on the PK of labetalol stereoisomers and the pharmacodynamic effects.	Labetalol	105-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
23230132-8	2013	All recombinant UGTs, except UGT1A1, 1A6, and 1A10, produced EtG in detectable amounts.	ethyl glucuronide	61-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
23237922-3	2013	Of these, 33 patients were subjected to HLA typing and polymorphism analyses of CYP3A5, ABCB1, ABCC2, and UGT1A1, which are involved in the metabolism and membrane transport of sorafenib.	Sorafenib	177-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
23488780-7	2013	Assessment of a panel of recombinant UGT isoforms revealed that UGT1A1, UGT1A3 and UGT1A9 could catalyse the glucuronidation of arbidol.	umifenovir	128-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	104-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	114-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23789755-1	2013	OBJECTIVE: To evaluate the influence of genetic polymorphism in UGT1A1, UGT1A7 and UGT1A9 on the population pharmacokinetics of irinotecan and its metabolites, SN-38 and SN-38G.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
23789755-7	2013	The presence of UGT1A1*28, UGT1A7*3, UGT1A9*22 genotypes decreases SN-38 clearance between 20 and 36%.	Irinotecan	67-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
23789755-9	2013	CONCLUSION: The inclusion of pharmacokinetic-pharmacogenomic information can add value to the individualized dose adjustment of irinotecan, because it will let quantitatively handle dose reductions in patients with iatrogenic toxicity due to UGT1A1 genetic polymorphisms.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	242-248
22813462-4	2013	Recombinant UGT isoforms screening experiment and enzyme kinetic study showed that UGT1A1 completely contributed to the glucuronidation of thienorphine.	thienorphine	139-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
23663345-0	2013	[Effects of autophagy modulator on autophagy and uridine 5"-diphospho-glucuronosyltransferase 1A1 induced by sulforaphane].	sulforaphane	109-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-97
23663345-1	2013	OBJECTIVE: To explore the effects of 3-methyladenine (3-MA) and rapamycin (Rapa) on autophagy and uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) induced by sulforaphane (SFN) in human colon cancer Caco-2 cells.	3-methyladenine	54-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-146
23663345-1	2013	OBJECTIVE: To explore the effects of 3-methyladenine (3-MA) and rapamycin (Rapa) on autophagy and uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) induced by sulforaphane (SFN) in human colon cancer Caco-2 cells.	sulforaphane	167-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-146
23663345-1	2013	OBJECTIVE: To explore the effects of 3-methyladenine (3-MA) and rapamycin (Rapa) on autophagy and uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) induced by sulforaphane (SFN) in human colon cancer Caco-2 cells.	sulforaphane	181-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-146
23663345-13	2013	And Rapa also potentiates SFN-induced UGT1A1 expression.	sulforaphane	26-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
22934695-2	2013	This study aims to investigate the association between UGT1A1 gene polymorphisms and irinotecan related toxicities in Chinese Han gastrointestinal cancer patients receiving FOLFIRI regimen chemotherapy.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
22934695-2	2013	This study aims to investigate the association between UGT1A1 gene polymorphisms and irinotecan related toxicities in Chinese Han gastrointestinal cancer patients receiving FOLFIRI regimen chemotherapy.	FOLFIRI regimen	173-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
22934695-12	2013	The baseline serum total bilirubin was elevated in UGT1A1*28, *93 allele carriers and *60 homozygote, but with no relationship with severe toxicities.	Bilirubin	25-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
23132334-5	2013	UDP-glucuronosyltransferase (UGT) 1A1 is the main enzyme responsible for the metabolism of DTG in vivo, with cytochrome P450 (P450) 3A4 being a notable pathway and UGT1A3 and UGT1A9 being only minor pathways.	dolutegravir	91-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23148286-0	2013	Impact of UGT1A1 Gilbert variant on discontinuation of ritonavir-boosted atazanavir in AIDS Clinical Trials Group Study A5202.	Ritonavir	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
23148286-0	2013	Impact of UGT1A1 Gilbert variant on discontinuation of ritonavir-boosted atazanavir in AIDS Clinical Trials Group Study A5202.	Atazanavir Sulfate	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
23148286-1	2013	The UGT1A1*28 variant has been associated with hyperbilirubinemia and atazanavir discontinuation.	Atazanavir Sulfate	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
23303296-12	2013	In conclusion, UGT1A1*6/*28, UGT1A7*3/*3, and UGT1A9*1/*1 should be taken into consideration as markers for preventing severe adverse events of CPT-11 administration.	Irinotecan	144-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
23277092-4	2013	RESULTS: Two haplotypes in UGT1A1/UGT1A8 were weak predictors of reduced M6G/morphine and M3G/morphine serum ratios after oral administration (false discovery rate-corrected P-values&lt;0.1).	Morphine	77-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
23277092-4	2013	RESULTS: Two haplotypes in UGT1A1/UGT1A8 were weak predictors of reduced M6G/morphine and M3G/morphine serum ratios after oral administration (false discovery rate-corrected P-values&lt;0.1).	Morphine	94-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
23148825-0	2013	Protein-protein interactions between the bilirubin-conjugating UDP-glucuronosyltransferase UGT1A1 and its shorter isoform 2 regulatory partner derived from alternative splicing.	Bilirubin	41-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
23148825-4	2013	The bilirubin-conjugating UGT1A1 was used as a prototype.	Bilirubin	4-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
23388413-2	2013	Among the UGT gene family members, only UGT1A1 is involved in bilirubin conjugation.	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
23130636-2	2013	UGT1A1 (UDP-glucuronosyltransferase 1A1) is a critical gene for bilirubin metabolism and irinotecan detoxification.	Bilirubin	64-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23130636-2	2013	UGT1A1 (UDP-glucuronosyltransferase 1A1) is a critical gene for bilirubin metabolism and irinotecan detoxification.	Bilirubin	64-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
23130636-2	2013	UGT1A1 (UDP-glucuronosyltransferase 1A1) is a critical gene for bilirubin metabolism and irinotecan detoxification.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23130636-2	2013	UGT1A1 (UDP-glucuronosyltransferase 1A1) is a critical gene for bilirubin metabolism and irinotecan detoxification.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
23089672-11	2013	Regarding phase II enzyme polymorphism, the anticancer treatment with mercaptopurines and irinotecan is still considered important in relation to the polymorphism of TPMT and UGT1A1, respectively.	Mercaptopurine	70-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	175-181
23089672-11	2013	Regarding phase II enzyme polymorphism, the anticancer treatment with mercaptopurines and irinotecan is still considered important in relation to the polymorphism of TPMT and UGT1A1, respectively.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	175-181
24390949-3	2013	Thymine-adenine (TA)  repeats in the promoter region of UGT1A1 gene investigated by means of  polymerase- chain reaction (PCR) DNA sequencing.	thymine-adenine	0-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
23036853-8	2013	Among the enzymes catalyzing BaP oxidation and conjugation, cytochrome P450 1A1, 1A2, 3A4 and UDP-glucuronosyltransferase 1A1 mRNAs were induced by the exposure to TCDD.	Benzo(a)pyrene	29-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-125
23036853-8	2013	Among the enzymes catalyzing BaP oxidation and conjugation, cytochrome P450 1A1, 1A2, 3A4 and UDP-glucuronosyltransferase 1A1 mRNAs were induced by the exposure to TCDD.	Polychlorinated Dibenzodioxins	164-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-125
23147267-0	2013	UDP-glucuronosyltransferase 1A1 (UGT1A1) gene haplotypes and their effect on serum bilirubin concentration in healthy Indian adults.	Bilirubin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
23147267-0	2013	UDP-glucuronosyltransferase 1A1 (UGT1A1) gene haplotypes and their effect on serum bilirubin concentration in healthy Indian adults.	Bilirubin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
23147267-1	2013	The aim of the present study was to investigate the allele and genotype frequencies and haplotype structures of the variants in the UGT1A1 gene and their association with serum bilirubin levels in healthy adults.	Bilirubin	177-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
23147267-7	2013	Promoter polymorphisms and a common haplotype of the UGT1A1 gene are associated with serum bilirubin concentrations and could be a genetic risk factor for hyperbilirubinemia in Indians.	Bilirubin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
24390949-3	2013	Thymine-adenine (TA)  repeats in the promoter region of UGT1A1 gene investigated by means of  polymerase- chain reaction (PCR) DNA sequencing.	Tantalum	17-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
23089802-3	2013	Impaired or reduced UGT1A1 activity causes unconjugated hyperbilirubinemia (Gilbert"s syndrome and Crigler-Najjar syndrome) and side effects of drug treatment such as SN-38 (active metabolite of the anticancer drug irinotecan)-induced toxicity.	Irinotecan	215-225	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23449330-7	2013	E-3OH and SN-38 glucuronidation by recombinant hUGT1A1 and mpUGT1A1 showed allosteric sigmoidal kinetics.	3oh	2-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-54
23449330-7	2013	E-3OH and SN-38 glucuronidation by recombinant hUGT1A1 and mpUGT1A1 showed allosteric sigmoidal kinetics.	Irinotecan	10-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-54
23264445-1	2013	BACKGROUND: Homozygosity for UGT1A1*28/*28 has been reported to be associated with atazanavir-associated hyperbilirubinaemia and premature atazanavir discontinuation.	Atazanavir Sulfate	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
23264445-1	2013	BACKGROUND: Homozygosity for UGT1A1*28/*28 has been reported to be associated with atazanavir-associated hyperbilirubinaemia and premature atazanavir discontinuation.	Atazanavir Sulfate	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
23264445-4	2013	We assumed the UGT1A1-associated atazanavir discontinuation rate reported in the Swiss HIV Cohort Study (a *28/*28 frequency of 14.9%), equal efficacy and cost of atazanavir and darunavir and a genetic assay cost of $107.	Atazanavir Sulfate	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
23449330-5	2013	Then the kinetics of estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation by recombinant UGT1A1s as well as human and minipig liver microsomes were analyzed.	Estradiol	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
23449330-5	2013	Then the kinetics of estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation by recombinant UGT1A1s as well as human and minipig liver microsomes were analyzed.	3oh	56-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
23449330-5	2013	Then the kinetics of estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation by recombinant UGT1A1s as well as human and minipig liver microsomes were analyzed.	Irinotecan	65-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
23449330-5	2013	Then the kinetics of estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation by recombinant UGT1A1s as well as human and minipig liver microsomes were analyzed.	Irinotecan	97-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
23053265-0	2013	Uridine diphosphate glucuronosyl transferase 1 family polypeptide A1 gene (UGT1A1) polymorphisms are associated with toxicity and efficacy in irinotecan monotherapy for refractory pancreatic cancer.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
23089802-1	2013	Human UDP-glucuronosyltransferase (UGT) 1A1 is the enzyme that detoxifies neurotoxic bilirubin by conjugating it with glucuronic acid.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
23089802-1	2013	Human UDP-glucuronosyltransferase (UGT) 1A1 is the enzyme that detoxifies neurotoxic bilirubin by conjugating it with glucuronic acid.	Glucuronic Acid	118-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
23089802-3	2013	Impaired or reduced UGT1A1 activity causes unconjugated hyperbilirubinemia (Gilbert"s syndrome and Crigler-Najjar syndrome) and side effects of drug treatment such as SN-38 (active metabolite of the anticancer drug irinotecan)-induced toxicity.	Irinotecan	167-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23781580-0	2013	UGT1A1 genotype-specific phase I and pharmacokinetic study for combination chemotherapy with irinotecan and cisplatin: a Saitama Tumor Board study.	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23648677-3	2013	A study using UGT-expressing supersomes revealed that sipoglitazar glucuronidation was more extensively catalyzed by UGT1A1, 1A3, 1A6, 2B4, and 2B15 than by other UGTs.	sipoglitazar	54-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
23648677-5	2013	In a correlation study between sipoglitazar glucuronidation and UGT isoform-specific activities, the glucuronidation of S-oxazepam, a specific substrate for UGT2B15, strongly correlated with that of sipoglitazar, as compared with that of beta-estradiol, a representative UGT1A1 substrate.	sipoglitazar	31-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
23648677-5	2013	In a correlation study between sipoglitazar glucuronidation and UGT isoform-specific activities, the glucuronidation of S-oxazepam, a specific substrate for UGT2B15, strongly correlated with that of sipoglitazar, as compared with that of beta-estradiol, a representative UGT1A1 substrate.	Oxazepam	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
23648677-5	2013	In a correlation study between sipoglitazar glucuronidation and UGT isoform-specific activities, the glucuronidation of S-oxazepam, a specific substrate for UGT2B15, strongly correlated with that of sipoglitazar, as compared with that of beta-estradiol, a representative UGT1A1 substrate.	sipoglitazar	199-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
23781580-0	2013	UGT1A1 genotype-specific phase I and pharmacokinetic study for combination chemotherapy with irinotecan and cisplatin: a Saitama Tumor Board study.	Cisplatin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23781580-2	2013	The aim of the present study was to determine the RD of irinotecan in combination with cisplatin (CPT-P) for individuals with or without UGT1A1 polymorphisms.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
23781580-8	2013	CONCLUSION: UGT1A1 genotype-based RDs of irinotecan in CPT-P therapy were determined.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23781580-8	2013	CONCLUSION: UGT1A1 genotype-based RDs of irinotecan in CPT-P therapy were determined.	cpt	55-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23781580-8	2013	CONCLUSION: UGT1A1 genotype-based RDs of irinotecan in CPT-P therapy were determined.	Phosphorus	56-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
22805420-7	2013	UGT1A1 rs6742078 TT versus GG genotype was associated with 95% increased bilirubin levels (P &lt; 0.001); TT versus GG genotype was associated with odds ratios (ORs) of 1.03 (95% CI, 0.96-1.11; P = 0.73) for IHD and 1.01 (95% CI, 0.92-1.12; P = 0.68) for MI.	Bilirubin	73-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23237733-2	2013	Therefore, the aim of the present study was to investigate the inhibition of isoliquiritigenin towards important UGT isoforms in the liver and intestine, including UGT1A1, 1A3, 1A6, 1A7, 1A8, 1A9 and 1A10.	isoliquiritigenin	77-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
23237733-4	2013	The results showed that 100muM of isoliquiritigenin inhibited the activity of UGT1A1, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A9, and UGT1A10 by 95.2%, 76.1%, 78.9%, 87.2%, 67.2%, 94.8%, and 91.7%, respectively.	isoliquiritigenin	34-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
23783485-0	2013	Associations between UGT1A1*6/*28 polymorphisms and irinotecan-induced severe toxicity in Chinese gastric or esophageal cancer patients.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
23686699-0	2013	UGT1A1 6/28 polymorphisms could predict irinotecan-induced severe neutropenia not diarrhea in Chinese colorectal cancer patients.	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23783485-1	2013	The aim of this study was to investigate the associations between UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms and irinotecan-induced toxicities in Chinese advanced gastric or esophageal cancer patients.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-103
23686699-1	2013	The aim of this study was to investigate the associations between UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms and irinotecan-induced toxicities in Chinese advanced colorectal cancer patients.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-103
23686699-9	2013	Both UGT1A1 6 and UGT1A1 28 variants were closely associated with irinotecan-induced severe neutropenia, but not diarrhea.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
23236239-0	2012	UGT1A1 predicts outcome in colorectal cancer treated with irinotecan and fluorouracil.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23686699-9	2013	Both UGT1A1 6 and UGT1A1 28 variants were closely associated with irinotecan-induced severe neutropenia, but not diarrhea.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
23516488-0	2013	Association between UGT1A1*28 polymorphisms and clinical outcomes of irinotecan-based chemotherapies in colorectal cancer: a meta-analysis in Caucasians.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23516488-1	2013	BACKGROUND: Whether UGT1A1*28 genotype is associated with clinical outcomes of irinotecan (IRI)-based chemotherapy in Colorectal cancer (CRC) is an important gap in existing knowledge to inform clinical utility.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23382909-5	2013	The major pathway of metabolism involves UGT1A1-mediated glucuronidation and a good correlation has been identified between belinostat glucuronide formation and glucuronidation of known UGT1A1 substrates.	Belinostat glucuronide	124-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
23382909-5	2013	The major pathway of metabolism involves UGT1A1-mediated glucuronidation and a good correlation has been identified between belinostat glucuronide formation and glucuronidation of known UGT1A1 substrates.	Belinostat glucuronide	124-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-192
23382909-7	2013	The main metabolic pathway of belinostat is through glucuronidation mediated primarily by UGT1A1, a highly polymorphic enzyme.	belinostat	30-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
23236239-0	2012	UGT1A1 predicts outcome in colorectal cancer treated with irinotecan and fluorouracil.	Fluorouracil	73-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23236239-9	2012	Differences in irinotecan and its metabolites between UGT1A1 gene variants were compared.	Irinotecan	15-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
23236239-21	2012	Irinotecan PK was investigated in 34 patients, which showed high area under concentration curve (AUC) of irinotecan and SN-38, but low AUC ratio (SN-38G / SN-38) in those patients with UGT1A1*28 TA7/7.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
23236239-22	2012	CONCLUSION: A distinct distribution pattern of UGT1A1 genotypes in Chinese patients might contribute to relatively low toxicity associated with irinotecan and 5-fluorouracil in mCRC patients.	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
23236239-22	2012	CONCLUSION: A distinct distribution pattern of UGT1A1 genotypes in Chinese patients might contribute to relatively low toxicity associated with irinotecan and 5-fluorouracil in mCRC patients.	Fluorouracil	159-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
23279026-4	2012	It is well-known that UGT1A1, UGT1A6 and UGT1A9 enzymes glucuronidate acetaminophen.	Acetaminophen	70-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	glycitein	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	Sulfates	62-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	glycitein	220-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	Isoflavones	277-288	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	Sulfates	292-300	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	Sulfates	292-300	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	Glucuronides	339-350	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-5	2012	UGT1A1*28 was associated only with percentage of glycitein as sulphate (positive; p = 0.046), but excluding five participants with both minor alleles of CBG and ABCG2 uncovered additional associations with percentage of glycitein as glucuronide (negative; p = 0.028), combined isoflavones as sulphate (positive; p = 0.035) and sulphate-to-glucuronide ratio for combined isoflavones (positive; p = 0.036).	Isoflavones	370-381	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23097198-7	2012	CONCLUSION: Genetic variation in UGT1A1, CBG, ABCG2, and ABCC2 influences isoflavone metabolism so may affect benefits of dietary consumption.	Isoflavones	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
23207817-1	2012	Bilirubin is conjugated with glucoronic acid in the liver by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-92
23233861-7	2012	Of the proposed gene/drug pairs the highest importance was assigned to HLA-B/abacavir, UGT1A1/irinotecan, and CYP2D6/tamoxifen.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
23207817-1	2012	Bilirubin is conjugated with glucoronic acid in the liver by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
23207817-1	2012	Bilirubin is conjugated with glucoronic acid in the liver by UDP-glucuronosyltransferase 1A1 (UGT1A1).	glucoronic acid	29-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-92
23207817-1	2012	Bilirubin is conjugated with glucoronic acid in the liver by UDP-glucuronosyltransferase 1A1 (UGT1A1).	glucoronic acid	29-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
23323463-8	2012	The prodrug irinotecan is biotransformed by carboxylesterase into its active metabolite SN-38, which is inactivated by UGT1 into the inactive compound SN-38G.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-123
22648071-0	2012	UDP-glucuronosyltransferase 1A1 is the principal enzyme responsible for puerarin metabolism in human liver microsomes.	puerarin	72-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
22648071-6	2012	In vitro, we used a UDP-glucuronosyltransferase (UGT) reaction screening method with 12 recombinant human UGTs to demonstrate that formation of puerarin-7-O-glucuronide was catalyzed by UGT1A1, 1A9, 1A10, 1A3, 1A6, 1A7, and 1A8.	puerarin-7-O-glucuronide	144-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-192
22648071-7	2012	UGT1A1, 1A9, and 1A10 significantly catalyzed puerarin-7-O-glucuronide formation, and the activity of UGT1A1 was significantly higher than those of 1A9 and 1A10.	puerarin-7-O-glucuronide	46-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22648071-9	2012	The kinetics of puerarin-7-O-glucuronide formation catalyzed by UGT1A1 were similar to those of the pooled human liver microsomes (HLMs), with V                 (max) values of 186.3 and 149.2 pmol/min/mg protein, and K                 (                   m                 ) values of 811.3 and 838.9 muM, respectively.	puerarin-7-O-glucuronide	16-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
22648071-10	2012	Furthermore, bilirubin and beta-estradiol, probe substrates for UGT1A1, significantly inhibited the formation of puerarin-7-O-glucuronide in HLMs.	Bilirubin	13-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
22648071-10	2012	Furthermore, bilirubin and beta-estradiol, probe substrates for UGT1A1, significantly inhibited the formation of puerarin-7-O-glucuronide in HLMs.	Estradiol	27-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
22648071-10	2012	Furthermore, bilirubin and beta-estradiol, probe substrates for UGT1A1, significantly inhibited the formation of puerarin-7-O-glucuronide in HLMs.	puerarin-7-O-glucuronide	113-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
22829544-1	2012	Human UDP-glucuronosyltransferase (UGT) 1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds such as bilirubin.	Bilirubin	168-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
22829544-2	2012	The present study shows how cyclin-dependent kinase (CDK) inhibitor roscovitine stimulated the expression of UGT1A1 in HepG2 cells.	Roscovitine	68-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
22829544-3	2012	Pregnane X receptor (PXR)-mediated transactivation of UGT1A1 reporter gene was more prominently enhanced by roscovitine, compared with the basal-, constitutive androstane receptor (CAR)-, and aryl hydrocarbon receptor-mediated activities.	Roscovitine	108-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
22829544-4	2012	We determined the regulatory mechanism of UGT1A1 expression through PXR"s stimulation by roscovitine.	Roscovitine	89-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
22829544-5	2012	Although phosphomimetic mutations at Thr290 and Thr408 retained the PXR protein in cytoplasm and attenuated the induction of UGT1A1 expression by both roscovitine and rifampicin, a mutation at Ser350 specifically reduced the activity of PXR induced by roscovitine.	Roscovitine	151-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
22829544-5	2012	Although phosphomimetic mutations at Thr290 and Thr408 retained the PXR protein in cytoplasm and attenuated the induction of UGT1A1 expression by both roscovitine and rifampicin, a mutation at Ser350 specifically reduced the activity of PXR induced by roscovitine.	Rifampin	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
22829544-5	2012	Although phosphomimetic mutations at Thr290 and Thr408 retained the PXR protein in cytoplasm and attenuated the induction of UGT1A1 expression by both roscovitine and rifampicin, a mutation at Ser350 specifically reduced the activity of PXR induced by roscovitine.	Roscovitine	252-263	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
22829544-10	2012	These results indicate that roscovitine stimulated the expression of UGT1A1 by inhibiting CDK2, which phosphorylated PXR at Ser350 to suppress binding with RXR and coactivator and maintain the acetylation of PXR protein.	Roscovitine	28-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
22820246-2	2012	For examples: (i) bilirubin is solely conjugated by UGT1A1 and activates its transcription factors Ah receptor, PXR and CAR.	Bilirubin	18-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
22212955-0	2012	Association of serum bilirubin and promoter variations in HMOX1 and UGT1A1 genes with sporadic colorectal cancer.	Bilirubin	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
22212955-1	2012	Heme oxygenase-1 (HMOX1) and bilirubin UDP-glucuronosyltransferase (UGT1A1) enzymes, both involved in bilirubin homeostasis, play an important role in the oxidative stress defense.	Bilirubin	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
22212955-4	2012	The (GT)(n)  and (TA)(n)  dinucleotide variations in HMOX1 and UGT1A1 gene promoters, respectively, were determined by fragment analysis.	(n)  dinucleotide	21-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
23323463-8	2012	The prodrug irinotecan is biotransformed by carboxylesterase into its active metabolite SN-38, which is inactivated by UGT1 into the inactive compound SN-38G.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-123
23323463-8	2012	The prodrug irinotecan is biotransformed by carboxylesterase into its active metabolite SN-38, which is inactivated by UGT1 into the inactive compound SN-38G.	Irinotecan	151-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-123
22050734-3	2012	Some protease inhibitors (mainly atazanavir and indinavir) act as inhibitors of uridine diphosphate-glucuronosyltransferase (UGT1A1), the enzyme responsible for hepatic conjugation of bilirubin.	Atazanavir Sulfate	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
22910411-3	2012	Using HepG2 cells expressing human CAR in the presence of tetracycline, we showed that knockdown of DP97 with small interfering RNAs suppressed tetracycline-inducible mRNA expression of CYP2B6 and UGT1A1 but not CYP3A4.	Tetracycline	144-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	197-203
22050734-3	2012	Some protease inhibitors (mainly atazanavir and indinavir) act as inhibitors of uridine diphosphate-glucuronosyltransferase (UGT1A1), the enzyme responsible for hepatic conjugation of bilirubin.	Indinavir	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
22050734-3	2012	Some protease inhibitors (mainly atazanavir and indinavir) act as inhibitors of uridine diphosphate-glucuronosyltransferase (UGT1A1), the enzyme responsible for hepatic conjugation of bilirubin.	Bilirubin	184-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
22050734-4	2012	Variations in the promoter region of the UGT1A1 gene (UGT1A1*28, rs8175347) can influence bilirubin plasma levels, modulating the susceptibility to hyperbilirubinemia.	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
22050734-4	2012	Variations in the promoter region of the UGT1A1 gene (UGT1A1*28, rs8175347) can influence bilirubin plasma levels, modulating the susceptibility to hyperbilirubinemia.	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
22050734-6	2012	Individuals carrying the UGT1A1*28 allele had a higher risk of developing severe hyperbilirubinemia [prevalence ratio (PR)=2.43, 95% confidence interval (CI) 1.08-5.45, p=0.032] as well as atazanavir users (PR=7.72, 95% CI=3.14-18.98, p&lt;0.001).	Atazanavir Sulfate	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
22050734-7	2012	This is the first description of such an association in Brazilian HIV patients, which shows that in African-American and Euroamerican HAART users, the UGT1A1*28 allele also predisposes to severe hyperbilirubinemia, especially in those exposed to atazanavir.	Atazanavir Sulfate	246-256	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
22661571-5	2012	RESULTS: At baseline, UGT1A1 heterozygous and homozygous patients had significantly higher bilirubin levels than wild-type (P = 0.012 and P &lt; 0.001, respectively).	Bilirubin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
22661571-9	2012	CONCLUSIONS: UGT1A1*28 is significantly related to hyperbilirubinaemia in HIV-1 patients receiving atazanavir.	Atazanavir Sulfate	99-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
22661571-11	2012	Unboosted atazanavir-containing therapy is safe and efficacious in patients with an undetectable viral load with a UGT1A1*28 polymorphism, allowing the use of atazanavir in patients otherwise likely unable to receive it.	Atazanavir Sulfate	10-20	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
22661630-6	2012	The expression of UGT1A1 v2/v3 was 1.6-fold higher than v1 (p = 0.03) in HepG2 cells, and short interfering RNA knockdown of HepG2 v2/v3 increased raloxifene glucuronidation activity by 83%.	Raloxifene Hydrochloride	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
22435749-3	2012	Unique tryptic peptides of UGT1A1 and UGT2B7 in tryptically digested HLMs were simultaneously quantified by liquid chromatography (LC) equipped with tandem mass spectrometry (MS) using corresponding stable isotope-labelled peptides as internal standards.	Peptides	15-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
23016456-4	2012	Among the tested UGT isoforms, UGT1A1, UGT1A3, UGT2B7 and UGT2B15 were strongly inhibited by tacro in a concentration-dependent manner.	Tacrolimus	93-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
22435749-3	2012	Unique tryptic peptides of UGT1A1 and UGT2B7 in tryptically digested HLMs were simultaneously quantified by liquid chromatography (LC) equipped with tandem mass spectrometry (MS) using corresponding stable isotope-labelled peptides as internal standards.	Peptides	223-231	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
22749334-0	2012	Effects of statin treatments and polymorphisms in UGT1A1 and SLCO1B1 on serum bilirubin levels in Chinese patients with hypercholesterolaemia.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
21978357-1	2012	Raltegravir is metabolized by glucuronidation via UDP-glucuronosyltransferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-81
21978357-1	2012	Raltegravir is metabolized by glucuronidation via UDP-glucuronosyltransferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
21978357-2	2012	We analyzed the genotypes of UGT1A1 (*6, *27, and *28) and their contribution to plasma raltegravir concentrations in 56 Japanese HIV-1-infected patients in the National Hospital Organization Nagoya Medical Center of Japan.	Raltegravir Potassium	88-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
21978357-9	2012	However, variability in raltegravir concentration and small patient population precluded a correlation between UGT1A1*6 homozygosity and plasma raltegravir concentration.	Raltegravir Potassium	144-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
21978357-10	2012	To clarify the contribution of UGT1A1*6 or *28 polymorphisms to plasma raltegravir concentrations, further investigations on larger subject populations are required.	Raltegravir Potassium	71-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
22749334-2	2012	The organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) and UDP-glucuronosyltransferase 1A1 (UGT1A1) play an important role in the disposition of bilirubin.	Bilirubin	161-170	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-106
22749334-2	2012	The organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) and UDP-glucuronosyltransferase 1A1 (UGT1A1) play an important role in the disposition of bilirubin.	Bilirubin	161-170	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
22749334-4	2012	METHODS: Associations between common polymorphisms in UGT1A1 and SLCO1B1 and the serum bilirubin levels on no lipid-lowering treatment were analyzed in 379 Chinese patients with hypercholesterolaemia.	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
22749334-6	2012	RESULTS: The UGT1A1 polymorphisms associated with reduced enzyme activity were significantly associated with increased baseline bilirubin levels.	Bilirubin	128-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
22749334-9	2012	CONCLUSIONS: This study showed that the polymorphisms in UGT1A1, but not SLCO1B1, were associated with serum bilirubin levels in Chinese patients.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
22943620-4	2012	In a recombinant human UGT1A1 assay, the assay buffer components uridine and its phosphorylated derivatives are isobaric with RBV and its phosphorylated metabolites, leading to significant interference when analyzed by LC-MS with the nominal mass resolution mode.	Uridine	65-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
22943620-4	2012	In a recombinant human UGT1A1 assay, the assay buffer components uridine and its phosphorylated derivatives are isobaric with RBV and its phosphorylated metabolites, leading to significant interference when analyzed by LC-MS with the nominal mass resolution mode.	Ribavirin	126-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
22943620-6	2012	CONCLUSION: The developed LC-high-resolution accurate MS method allows for quantitation of RBV and its phosphorylated metabolites, eliminating the interferences from uridine and its phosphorylated derivatives in recombinant human UGT1A1 assays.	Ribavirin	91-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
22960892-1	2012	BACKGROUND &amp; OBJECTIVES: Genetic polymorphisms of uridine diphosphate glucuronyltransferase 1A1 (UGT1A1) have been associated with a wide variation of responses among patients prescribed with irinotecan.	Adenosine Monophosphate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-1	2012	BACKGROUND &amp; OBJECTIVES: Genetic polymorphisms of uridine diphosphate glucuronyltransferase 1A1 (UGT1A1) have been associated with a wide variation of responses among patients prescribed with irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-11	2012	INTERPRETATION &amp; CONCLUSIONS: There was interethnic variability in the frequency of UGT1A1*28 in the Malaysian population.	Adenosine Monophosphate	16-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
22960892-12	2012	Our results suggest that genotyping of UUGT1A1*6, UGT1A1*28 and UGT1A1*27 need to be performed before patients are prescribed with irinotecan due to their high prevalence of allelic variant which could lead to adverse drug reaction.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
22565219-7	2012	UGT1A1 showed a 2.1-fold (P &lt;0.0001) higher V(max)/K(M) for formation of the CLZ-N+-glucuronide than UGT1A4; UGT1A4 was the only UGT for which CLZ-5-N-glucuronide kinetics could be determined.	clozapine N-glucuronide	80-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22957438-3	2012	The results showed that 100 microM of glimepiride inhibited UGT1A1, UGT1A3, UGT1A6, UGT1A9, UGT2B7 and UGT2B15 by 54.7%, 43.1%, 100%, 70.5%, 32.7 and 37.2%, respectively.	glimepiride	38-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
22565219-7	2012	UGT1A1 showed a 2.1-fold (P &lt;0.0001) higher V(max)/K(M) for formation of the CLZ-N+-glucuronide than UGT1A4; UGT1A4 was the only UGT for which CLZ-5-N-glucuronide kinetics could be determined.	clz-5-n-glucuronide	146-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22565219-10	2012	The UGT1A1*28 allele was a significant (P = 0.045) predictor of CLZ-N+-glucuronide formation; the UGT1A4*3 allele was a significant (P &lt; 0.0001) predictor of CLZ-5-N-glucuronide and dmCLZ-glucuronide formation.	clozapine N-glucuronide	64-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
22565219-11	2012	CONCLUSION: These data suggest that the UGT1A1*28 and UGT1A4*3 alleles contribute significantly to the interindividual variability in CLZ and dmCLZ metabolism.	Clozapine	134-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
22565219-11	2012	CONCLUSION: These data suggest that the UGT1A1*28 and UGT1A4*3 alleles contribute significantly to the interindividual variability in CLZ and dmCLZ metabolism.	norclozapine	142-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
22367021-12	2012	However, the predicted high activity UGT1A1 genotype, associated with low serum levels of the antioxidant bilirubin, was associated with an increased ESCC risk.	Bilirubin	106-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
22398043-3	2012	UDP-glucuronosyltransferase 1A1 (UGT1A1) is the only enzyme involved in the conjugation of bilirubin and the common UGT1A1*28 allele in the UGT1A1 gene, which is strongly associated with Gilbert"s syndrome in Caucasians, results in elevated plasma bilirubin levels.	Bilirubin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
22398043-3	2012	UDP-glucuronosyltransferase 1A1 (UGT1A1) is the only enzyme involved in the conjugation of bilirubin and the common UGT1A1*28 allele in the UGT1A1 gene, which is strongly associated with Gilbert"s syndrome in Caucasians, results in elevated plasma bilirubin levels.	Bilirubin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
22398043-3	2012	UDP-glucuronosyltransferase 1A1 (UGT1A1) is the only enzyme involved in the conjugation of bilirubin and the common UGT1A1*28 allele in the UGT1A1 gene, which is strongly associated with Gilbert"s syndrome in Caucasians, results in elevated plasma bilirubin levels.	Bilirubin	248-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
22398043-3	2012	UDP-glucuronosyltransferase 1A1 (UGT1A1) is the only enzyme involved in the conjugation of bilirubin and the common UGT1A1*28 allele in the UGT1A1 gene, which is strongly associated with Gilbert"s syndrome in Caucasians, results in elevated plasma bilirubin levels.	Bilirubin	248-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
22398043-3	2012	UDP-glucuronosyltransferase 1A1 (UGT1A1) is the only enzyme involved in the conjugation of bilirubin and the common UGT1A1*28 allele in the UGT1A1 gene, which is strongly associated with Gilbert"s syndrome in Caucasians, results in elevated plasma bilirubin levels.	Bilirubin	248-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
22398043-3	2012	UDP-glucuronosyltransferase 1A1 (UGT1A1) is the only enzyme involved in the conjugation of bilirubin and the common UGT1A1*28 allele in the UGT1A1 gene, which is strongly associated with Gilbert"s syndrome in Caucasians, results in elevated plasma bilirubin levels.	Bilirubin	248-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
22398043-10	2012	CONCLUSION: The homozygous state of the UGT1A1*28 polymorphism, associated with higher serum bilirubin levels, may be protective for the development of Crohn"s disease, suggesting that the anti-oxidant capacity of bilirubin may play a part.	Bilirubin	93-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
22398043-10	2012	CONCLUSION: The homozygous state of the UGT1A1*28 polymorphism, associated with higher serum bilirubin levels, may be protective for the development of Crohn"s disease, suggesting that the anti-oxidant capacity of bilirubin may play a part.	Bilirubin	214-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
22676194-0	2012	Impact of the UGT1A1*28 allele on response to irinotecan: a systematic review and meta-analysis.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
22676194-1	2012	AIM: Pre-emptive irinotecan dose reduction for UGT1A1*28 homozygotes may result in reduced risk of severe neutropenia and diarrhea.	Irinotecan	17-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
22676194-3	2012	Whether UGT1A1*28 genotype is associated with irinotecan response therefore is an important gap in existing knowledge to inform clinical utility.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
22676194-4	2012	MATERIALS &amp; METHODS: A systematic review and meta-analysis was performed to analyze the difference in objective response rate (ORR) between irinotecan-administered cancer patients with different UGT1A1*28 genotypes: *28/*28 (homozygous variant), *1/*28 (heterozygous variant) or *1/*1 (wild-type).	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
22676194-5	2012	The effect of irinotecan dose on the association between UGT1A1*28 and ORR was also assessed.	Irinotecan	14-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
22516947-0	2012	Phase II and UGT1A1 genotype study of irinotecan dose escalation as salvage therapy for advanced gastric cancer.	Irinotecan	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
22170007-1	2012	PURPOSE: Axitinib, an orally administered inhibitor of vascular endothelial growth factor 1, 2 and 3, is primarily metabolized by cytochrome P450 (CYP) 3A4/5 but is also a substrate for CYP1A2, CYP2C19, UDP-glucuronosyltransferase (UGT)1A1 and the drug transporters P-glycoprotein (encoded by the ABCB1 gene) and OATP1B1 (encoded by SLC01B1).	Axitinib	9-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	232-239
22427354-7	2012	Epithelial markers for cell proliferation (Ki-67), terminal differentiation (transglutaminase 1-TGase1) and glucuronidation (UDP-glucuronosyltransferase1A1-UGT1A1) exhibited fenretinide concentration-specific relationships (elevated TGase1 and UGT1A1 levels &lt;5 muM, reduced Ki-67 indices &gt;5 muM) relative to blank-treated epithelium.	Fenretinide	174-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-155
22321050-1	2012	We recently designed the CIME cocktail consisting of 10 drugs to assess the activity of the major human CYPs (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A), a phase II enzyme (UGT1A1/6/9), two drug transporters (P-gp and OATP1B1) and a component of the renal function ( Videau et al.	cime	25-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-191
22543504-0	2012	Gossypol exhibits a strong influence towards UDP-glucuronosyltransferase (UGT) 1A1, 1A9 and 2B7-mediated metabolism of xenobiotics and endogenous substances.	Gossypol	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-82
22543504-3	2012	In the present study, in vitro human liver microsomal incubation system supplemented with UDPGA was used to investigate the inhibition of gossypol towards UGT1A1, 1A9 and 2B7-mediated metabolism of xenobiotics and endogenous substances.	Gossypol	138-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
22543504-4	2012	Estradiol, the probe substrate of UGT1A1, was selected as representative endogenous substance.	Estradiol	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
22448797-2	2012	A polymorphism of the 5  end of the UGT1A1 gene promoter, a homozygous insertion of TA pairs (genotype UGT1A1*28/*28), results in a decrease in bilirubin glucuronidation activity and therefore leads to an increase in the level of unconjugated bilirubin (hyperbilirubinemia).	Bilirubin	144-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
22448797-2	2012	A polymorphism of the 5  end of the UGT1A1 gene promoter, a homozygous insertion of TA pairs (genotype UGT1A1*28/*28), results in a decrease in bilirubin glucuronidation activity and therefore leads to an increase in the level of unconjugated bilirubin (hyperbilirubinemia).	Bilirubin	144-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
22448797-2	2012	A polymorphism of the 5  end of the UGT1A1 gene promoter, a homozygous insertion of TA pairs (genotype UGT1A1*28/*28), results in a decrease in bilirubin glucuronidation activity and therefore leads to an increase in the level of unconjugated bilirubin (hyperbilirubinemia).	Bilirubin	243-252	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
22448797-2	2012	A polymorphism of the 5  end of the UGT1A1 gene promoter, a homozygous insertion of TA pairs (genotype UGT1A1*28/*28), results in a decrease in bilirubin glucuronidation activity and therefore leads to an increase in the level of unconjugated bilirubin (hyperbilirubinemia).	Bilirubin	243-252	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
22307138-11	2012	CONCLUSIONS: This pilot study indicates that genotype status of UGT1A1, UGT1A9, and ABCC2 and serum bilirubin concentration increases reflect abnormally high AUC in patients treated with sorafenib.	Sorafenib	187-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
22357454-2	2012	Lapatinib-associated Hy"s Law cases have been characterized using human leukocyte antigen (HLA) DQA1*02:01/DRB1*07:01 and Gilbert"s syndrome UGT1A1*28/*28 genotypes.	Lapatinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
22085899-0	2012	UGT1A1 is a major locus influencing bilirubin levels in African Americans.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22085899-11	2012	In summary, UGT1A1 is a major locus influencing bilirubin levels and the results of this study promise to contribute to understanding of the etiology and treatment of hyperbilirubinaemia in African-ancestry populations.	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
22537951-9	2012	The Arg allele frequency of the polymorphisms of UGT1A1 gene in the case group was significantly higher than in the control group (P&lt;0.01).	Arginine	4-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
22307138-0	2012	Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia.	Sorafenib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
22307138-1	2012	PURPOSE: Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase).	Sorafenib	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
22307138-1	2012	PURPOSE: Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase).	Sorafenib	61-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
22307138-2	2012	We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin concentration.	Sorafenib	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
22307138-2	2012	We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin concentration.	Sorafenib	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
22307138-2	2012	We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin concentration.	Sorafenib	124-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
22307138-2	2012	We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin concentration.	Sorafenib	124-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
22307138-2	2012	We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin concentration.	Bilirubin	192-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
22307138-3	2012	EXPERIMENTAL DESIGN: Inhibition of UGT1A1-mediated bilirubin glucuronidation by sorafenib was assessed in vitro.	Bilirubin	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
22307138-3	2012	EXPERIMENTAL DESIGN: Inhibition of UGT1A1-mediated bilirubin glucuronidation by sorafenib was assessed in vitro.	Sorafenib	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
22307138-6	2012	RESULTS: Sorafenib exhibited mixed-mode inhibition of UGT1A1-mediated bilirubin glucuronidation (IC(50) = 18 mumol/L; K(i) = 11.7 mumol/L) in vitro.	Sorafenib	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
22307138-6	2012	RESULTS: Sorafenib exhibited mixed-mode inhibition of UGT1A1-mediated bilirubin glucuronidation (IC(50) = 18 mumol/L; K(i) = 11.7 mumol/L) in vitro.	Bilirubin	70-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
22307138-9	2012	Sorafenib exposure was related to plasma bilirubin increases in patients carrying 1 or 2 copies of UGT1A1*28 alleles (n = 12 and n = 5; R(2) = 0.38 and R(2) = 0.77; P = 0.032 and P = 0.051, respectively).	Sorafenib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
22307138-10	2012	UGT1A1*28 carriers showed two distinct phenotypes that could be explained by ABCC2-24C&gt;T genotype and are more likely to experience plasma bilirubin increases following sorafenib if they had high sorafenib exposure.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22307138-10	2012	UGT1A1*28 carriers showed two distinct phenotypes that could be explained by ABCC2-24C&gt;T genotype and are more likely to experience plasma bilirubin increases following sorafenib if they had high sorafenib exposure.	Sorafenib	172-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22307138-10	2012	UGT1A1*28 carriers showed two distinct phenotypes that could be explained by ABCC2-24C&gt;T genotype and are more likely to experience plasma bilirubin increases following sorafenib if they had high sorafenib exposure.	Sorafenib	199-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
22021027-6	2012	Samples with higher concentrations of n-6 fatty acids produced a higher expression of UGT1A1 mRNA.	Fatty Acids, Omega-6	38-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
22416852-7	2012	Study subjects were genotyped at the UGT1A1*28 locus, which is strongly associated with bilirubin levels.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
21923755-4	2012	KEY RESULTS: Intracellular accumulation of ezetimibe was significantly lower in MDCK-OATP1B1-UGT1A1-MRP2 triple-transfected cells compared with all other cell lines.	Ezetimibe	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
21923755-5	2012	Considerably higher amounts of ezetimibe glucuronide were found in the apical compartment of MDCK-OATP1B1-UGT1A1-MRP2 monolayers compared with all other cell lines.	ezetimibe glucuronide	31-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
21923755-7	2012	Intracellular concentrations of etoposide equivalents (i.e. parent compound plus metabolites) were affected only to a minor extent by the absence or presence of OATP1B1/UGT1A1/MRP2.	Etoposide	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
21923755-8	2012	In contrast, apical accumulation of etoposide equivalents was significantly higher in monolayers of both cell lines expressing MRP2 (MDCK-OATP1B1-MRP2, MDCK-OATP1B1-UGT1A1-MRP2) compared with the single-transfected (OATP1B1) and the control cell line.	Etoposide	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
22180045-5	2012	Assays with recombinant human UDP-glucuronosyltransferase enzymes (UGTs) revealed that multiple UGT isoforms were involved in magnolol glucuronidation, including UGT1A1, -1A3, -1A7, -1A8, -1A9, -1A10, and -2B7.	magnolol	126-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
22297387-7	2012	Efavirenz (single dose) slightly increased ezetimibe absorption and markedly decreased exposure to ezetimibe-glucuronide (single dose and multiple dose), which may be explained by inhibition of UGT1A1 and ABCB1 (in vitro data).	efavirenz	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
22297387-7	2012	Efavirenz (single dose) slightly increased ezetimibe absorption and markedly decreased exposure to ezetimibe-glucuronide (single dose and multiple dose), which may be explained by inhibition of UGT1A1 and ABCB1 (in vitro data).	ezetimibe glucuronide	99-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
22154984-0	2012	Evaluation of bisphenol A glucuronidation according to UGT1A1*28 polymorphism by a new LC-MS/MS assay.	bisphenol A	14-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
22740978-0	2012	Correlation between plasma concentration ratios of SN-38 glucuronide and SN-38 and neutropenia induction in patients with colorectal cancer and wild-type UGT1A1 gene.	7-ethyl-10-hydroxycamptothecin glucuronide	51-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
22740978-0	2012	Correlation between plasma concentration ratios of SN-38 glucuronide and SN-38 and neutropenia induction in patients with colorectal cancer and wild-type UGT1A1 gene.	Irinotecan	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
22740978-3	2012	A total of 17 patients with colorectal cancer and wild-type UDP-glucuronosyltransferase (UGT)1A1 gene were enrolled and treated with CPT-11 as part of the FOLFIRI regimen [CPT-11 and fluorouracil (5-FU)].	Irinotecan	133-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-96
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	40-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	125-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
22347861-3	2012	Protection from cardiovascular disease is also observed in patients with Gilbert"s syndrome which is a disease characterized by mutations in hepatic UGT1A1, the enzyme responsible for the conjugation of bilirubin into the bile.	Bilirubin	203-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
22154984-8	2012	Since BPA is a UGT1A1 substrate, we postulated that the common UGT1A1*28 polymorphism influences BPA glucuronidation, and consequently, BPA detoxification.	bisphenol A	6-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
22154984-8	2012	Since BPA is a UGT1A1 substrate, we postulated that the common UGT1A1*28 polymorphism influences BPA glucuronidation, and consequently, BPA detoxification.	bisphenol A	6-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
22154984-8	2012	Since BPA is a UGT1A1 substrate, we postulated that the common UGT1A1*28 polymorphism influences BPA glucuronidation, and consequently, BPA detoxification.	bisphenol A	97-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
22154984-8	2012	Since BPA is a UGT1A1 substrate, we postulated that the common UGT1A1*28 polymorphism influences BPA glucuronidation, and consequently, BPA detoxification.	bisphenol A	97-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
22154984-8	2012	Since BPA is a UGT1A1 substrate, we postulated that the common UGT1A1*28 polymorphism influences BPA glucuronidation, and consequently, BPA detoxification.	bisphenol A	97-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
22154984-8	2012	Since BPA is a UGT1A1 substrate, we postulated that the common UGT1A1*28 polymorphism influences BPA glucuronidation, and consequently, BPA detoxification.	bisphenol A	97-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
21760472-0	2012	Bilirubin dependence on UGT1A1 polymorphisms, hemoglobin, fasting time and body mass index.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
21760472-2	2012	This study evaluates how several nongenetic causes and the genetic UGT1A1 polymorphisms contribute for bilirubin levels, in a cohort of 146 young Caucasian females.	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
21953915-6	2012	Among the tested human UGT isoforms, UGT1A7, UGT1A8, and UGT1A9 showed the highest activity for the conjugation of hydroxylated TCC metabolites followed by UGT1A1, UGT1A3, and UGT1A10.	triclocarban	128-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
22252501-6	2012	Efavirenz also moderately inhibited UGT1A1-mediated 17beta-estradiol 3-glucuronidation, with a K(i) value of 40.3 muM, but did not inhibit UGT1A6-mediated 1-naphthol glucuronidation.	efavirenz	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
22252501-6	2012	Efavirenz also moderately inhibited UGT1A1-mediated 17beta-estradiol 3-glucuronidation, with a K(i) value of 40.3 muM, but did not inhibit UGT1A6-mediated 1-naphthol glucuronidation.	Estradiol	52-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
22252501-6	2012	Efavirenz also moderately inhibited UGT1A1-mediated 17beta-estradiol 3-glucuronidation, with a K(i) value of 40.3 muM, but did not inhibit UGT1A6-mediated 1-naphthol glucuronidation.	1-naphthol	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
22293344-4	2012	The aim of this study was to clarify the mechanism of these phenomena in HLM and human intestinal microsomes (HIM) and its relevance to uridine 5"-diphosphate (UDP)-glucuronosyl transferase (UGT) 1A1, UGT2B4 and UGT2B7, which mainly metabolize carvedilol directly in phase II enzymes.	Carvedilol	244-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-199
22201120-2	2012	All patients harbored UDP-glucuronosyltransferase (UGT) 1A1*1/*1, *1/*6, or *1/*28 genotypes, which are associated with similar irinotecan pharmacokinetics and responses to FOLFIRI.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-59
22118420-0	2012	A genome-wide search for non-UGT1A1 markers associated with unconjugated bilirubin level reveals significant association with a polymorphic marker near a gene of the nucleoporin family.	Bilirubin	73-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
22118420-1	2012	Variants in the UGT1A1 gene and its promoter are known to determine levels of unconjugated bilirubin (UCB), but do not explain all cases of unconjugated hyperbilirubinemia.	Bilirubin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
22118420-1	2012	Variants in the UGT1A1 gene and its promoter are known to determine levels of unconjugated bilirubin (UCB), but do not explain all cases of unconjugated hyperbilirubinemia.	ucb	102-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
22447115-4	2012	When cells were treated with a typical CYP3A substrate (triazolam), CYP2C9 substrate (diclofenac) or UGT1A1 substrate (SN-38), large amounts of their metabolites were detected in the medium of cells cultured on micro-space cell culture plates.	Irinotecan	119-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Triazolam	34-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
22201120-2	2012	All patients harbored UDP-glucuronosyltransferase (UGT) 1A1*1/*1, *1/*6, or *1/*28 genotypes, which are associated with similar irinotecan pharmacokinetics and responses to FOLFIRI.	FOLFIRI regimen	173-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-59
22673034-5	2012	The levels of CYP1A1, CYP1A2, and UGT1A1 mRNA expression were increased by omeprazole and 3-methylcholanthrene.	Omeprazole	75-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
22572482-4	2012	Among the 12 human UGTs investigated, UGT1A1 and UGT1A9 were the major isoforms that catalyzed the glucuronidation of Sal A (K(m) values of 29.72 +- 2.20 and 24.40 +- 2.60 microM).	salvianolic acid A	118-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Diclofenac	45-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Ketoconazole	129-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Sulfaphenazole	162-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Ketoconazole	200-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
22572482-8	2012	Mefenamic acid inhibited Sal A glucuronidation in UGT1A1 and HLMs with IC(50) values of &gt;200 and 12.4 +- 2.2 microM, respectively.	Mefenamic Acid	0-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
22673034-5	2012	The levels of CYP1A1, CYP1A2, and UGT1A1 mRNA expression were increased by omeprazole and 3-methylcholanthrene.	Methylcholanthrene	90-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
22572482-8	2012	Mefenamic acid inhibited Sal A glucuronidation in UGT1A1 and HLMs with IC(50) values of &gt;200 and 12.4 +- 2.2 microM, respectively.	sal	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
22450351-0	2012	Non tumoral hyperserotoninaemia responsive to octreotide due to dual polymorphism in UGT1A1 and UGT1A6.	Octreotide	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
22548118-3	2012	DA-9701 and Corydalis tuber extract slightly inhibited UGT1A1-mediated etoposide glucuronidation, with 50% inhibitory concentration (IC(50)) values of 188 and 290 mug/mL, respectively.	etoposide glucuronidation	71-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
23964438-4	2012	It was demonstrated that the genetic variations cause a decrease in UGT1A1 activity in neonates, leading to an accumulation of unconjugated bilirubin in serum.	Bilirubin	140-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
22567180-3	2012	METHODS: A novel oligonucleotide microarray was developed to genotype 13 variations (DPYD*2, DPYD*5, DPYD*9, TYMS 6 bp Ins/Del, UGT1A1*6, UGT1A1*27, UGT1A1*28, GSTP1 Ile105Val, XRCC1 Arg399Gln, MTHFR C677T, MDR1 C3435T/A, MDR1 G2677A/T and ERCC1 C118T).	Oligonucleotides	17-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
22567180-3	2012	METHODS: A novel oligonucleotide microarray was developed to genotype 13 variations (DPYD*2, DPYD*5, DPYD*9, TYMS 6 bp Ins/Del, UGT1A1*6, UGT1A1*27, UGT1A1*28, GSTP1 Ile105Val, XRCC1 Arg399Gln, MTHFR C677T, MDR1 C3435T/A, MDR1 G2677A/T and ERCC1 C118T).	Oligonucleotides	17-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
22567180-3	2012	METHODS: A novel oligonucleotide microarray was developed to genotype 13 variations (DPYD*2, DPYD*5, DPYD*9, TYMS 6 bp Ins/Del, UGT1A1*6, UGT1A1*27, UGT1A1*28, GSTP1 Ile105Val, XRCC1 Arg399Gln, MTHFR C677T, MDR1 C3435T/A, MDR1 G2677A/T and ERCC1 C118T).	Oligonucleotides	17-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
22508373-0	2012	A phase I study of infusional 5-fluorouracil, leucovorin, oxaliplatin and irinotecan in Japanese patients with advanced colorectal cancer who harbor UGT1A1*1/*1,*1/*6 or *1/*28.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
23430851-2	2012	It is caused by deficiency of the liver enzyme responsible for bilirubin elimination, the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1; EC 2.4.1.17).	Bilirubin	63-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-137
23430851-2	2012	It is caused by deficiency of the liver enzyme responsible for bilirubin elimination, the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1; EC 2.4.1.17).	Bilirubin	63-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
21972237-6	2012	In particular, UGT1A1 and extrahepatic UGT1A10 have significantly higher capacities than other isoforms for S-7-hydroxywarfarin and R-7-hydroxywarfarin glucuronidation, respectively.	7-hydroxywarfarin	108-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21972237-6	2012	In particular, UGT1A1 and extrahepatic UGT1A10 have significantly higher capacities than other isoforms for S-7-hydroxywarfarin and R-7-hydroxywarfarin glucuronidation, respectively.	(R)-7-Hydroxywarfarin	132-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21972237-7	2012	Activity data generated using a set of well characterized human liver microsomes supported the recombinant enzyme data, suggesting an important (although not exclusive) role for UGT1A1 in glucuronidation of the main warfarin metabolites, including Rac-6- and 7-hydroxywarfarin and their R- and S-enantiomers in the liver.	Warfarin	216-224	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	178-184
21972237-8	2012	This is the first demonstration that the R- and S-enantiomers of hydroxywarfarins are glucuronidated, with significantly different enzymatic affinity and capacity, and supports the importance of UGT1A1 as the major hepatic isoform involved.	hydroxywarfarins	65-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	195-201
21937736-7	2011	The aim of our in vitro study was to explain the mechanism behind the observed influence of UGT1A1*28 polymorphism on raloxifene pharmacokinetics in a small-sized in vivo study (Br J Clin Pharmacol 67:437-444, 2009).	Raloxifene Hydrochloride	118-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
22558097-1	2012	Serum bilirubin levels have been associated with polymorphisms in the UGT1A1 promoter in normal populations and in patients with hemolytic anemias, including sickle cell anemia.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
22293705-0	2012	[Examination of factors affecting adverse reactions and dosage reduction in UGT1A1 genotyped patients: a retrospective survey of irinotecan].	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
22293705-1	2012	Our aim was to clarify the side effects of irinotecan which occurred in patients admitted to Showa University Hospital to investigate whether the UGT1A1 genetic polymorphism status was reflected in the discontinuation or dose reduction of irinotecan.	Irinotecan	239-249	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
22293705-8	2012	Our investigation confirmed that the UGT1A1 genetic polymorphism status of the patients was reflected in the discontinuance or dose reduction of irinotecan.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
21985641-5	2011	UGT1A1 activity correlation analyses using flavonoids-4"-O-glucuronidation vs beta-estradiol-3-glucuronidation (a well-recognized marker for UGT1A1) or vs SN-38 glucuronidation were performed using a bank of HLMs (n = 12) including three UGT1A1-genotyped HLMs (i.e., UGT1A1*1*1, UGT1A1*1*28, and UGT1A1*28*28).	Irinotecan	155-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	Flavonoids	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-38
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	Flavonoids	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	4"-o	173-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-38
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	4"-o	173-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	3',4'-dihydroxyflavonol	197-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-38
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	3',4'-dihydroxyflavonol	197-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	3,6,4"-thf	213-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-38
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	3,6,4"-thf	213-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	3-o	276-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-38
21985641-6	2011	The results showed that UGT1A1 and 1A9, followed by 1A7, were the main isoforms for glucuronidating the two flavonoids, where UGT1A1 accounted for 92 +- 7% and 91 +- 10% of 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF, respectively, and UGT1A9 accounted for most of the 3-O-glucuronidation.	3-o	276-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	4"-o	31-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	3',4'-dihydroxyflavonol	55-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	3,6,4"-thf	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	Estradiol	132-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	3-oh	143-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	Irinotecan	153-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21985641-9	2011	This study demonstrated for the first time that regioselective glucuronidation of flavonoids can be applied to probe hepatic UGT1A1 activity in vitro.	Flavonoids	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
21726413-7	2011	The V(max)  values for beta-estradiol of p.P364L-UGT1A1, 1A3, 1A7, 1A8 and 1A10 were 36.6%, 82.1%, 26.8%, 29.2% and 22.5%, respectively, of the corresponding wild-type.	Estradiol	23-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
21726413-8	2011	Glucuronidation activity towards acetaminophen of p.P364L-UGT1A1, 1A6, 1A7, 1A8, 1A9 and 1A10 was 50.3%, 46.4%, 17.2%, 44.1%, 5.0% and 42.8%, respectively, of wild-type.	Acetaminophen	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
21787264-5	2011	In this view, the uridine diphosphate glucuronosil transferase isoform 1A1 (UGT1A1) was associated with significant changes in disposition of CPT-11 and its metabolites, and consequently with treatment-induced toxicities.	Irinotecan	142-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-74
21787264-5	2011	In this view, the uridine diphosphate glucuronosil transferase isoform 1A1 (UGT1A1) was associated with significant changes in disposition of CPT-11 and its metabolites, and consequently with treatment-induced toxicities.	Irinotecan	142-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
22077505-3	2011	METHODS: Published papers and publicly accessible genomic databases were searched up to August 2009 to obtain allele and genotype frequencies for UGT1A1*6 and *28, two common variants of UGT1A1, a gene that encodes for a key enzyme in the pathway of irinotecan metabolism.	Irinotecan	250-260	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
22077505-3	2011	METHODS: Published papers and publicly accessible genomic databases were searched up to August 2009 to obtain allele and genotype frequencies for UGT1A1*6 and *28, two common variants of UGT1A1, a gene that encodes for a key enzyme in the pathway of irinotecan metabolism.	Irinotecan	250-260	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
22077505-6	2011	Indians are at an elevated risk of irinotecan-induced neutropenia associated with UGT1A1*28 compared with Chinese and Japanese, and at an even higher risk compared with North American Caucasians.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
22077505-7	2011	On the other hand, Chinese and Japanese are at an elevated risk of irinotecan-induced neutropenia associated with UGT1A1*6 relative to Indians in Singapore or North American Caucasians.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
21985641-2	2011	Here, regioselective glucuronidation of two flavonoids, 3,3",4"-trihydroxyflavone (3,3",4"-THF) and 3,6,4"-trihydroxyflavone (3,6,4"-THF), is used to probe the activity of hepatic UGT1A1.	Flavonoids	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
21985641-2	2011	Here, regioselective glucuronidation of two flavonoids, 3,3",4"-trihydroxyflavone (3,3",4"-THF) and 3,6,4"-trihydroxyflavone (3,6,4"-THF), is used to probe the activity of hepatic UGT1A1.	3',4'-dihydroxyflavonol	56-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
21985641-2	2011	Here, regioselective glucuronidation of two flavonoids, 3,3",4"-trihydroxyflavone (3,3",4"-THF) and 3,6,4"-trihydroxyflavone (3,6,4"-THF), is used to probe the activity of hepatic UGT1A1.	3',4'-dihydroxyflavonol	83-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
21985641-2	2011	Here, regioselective glucuronidation of two flavonoids, 3,3",4"-trihydroxyflavone (3,3",4"-THF) and 3,6,4"-trihydroxyflavone (3,6,4"-THF), is used to probe the activity of hepatic UGT1A1.	3,6,4'-trihydroxyflavone	100-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
21985641-5	2011	UGT1A1 activity correlation analyses using flavonoids-4"-O-glucuronidation vs beta-estradiol-3-glucuronidation (a well-recognized marker for UGT1A1) or vs SN-38 glucuronidation were performed using a bank of HLMs (n = 12) including three UGT1A1-genotyped HLMs (i.e., UGT1A1*1*1, UGT1A1*1*28, and UGT1A1*28*28).	Flavonoids	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21985641-5	2011	UGT1A1 activity correlation analyses using flavonoids-4"-O-glucuronidation vs beta-estradiol-3-glucuronidation (a well-recognized marker for UGT1A1) or vs SN-38 glucuronidation were performed using a bank of HLMs (n = 12) including three UGT1A1-genotyped HLMs (i.e., UGT1A1*1*1, UGT1A1*1*28, and UGT1A1*28*28).	4"-o	54-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21985641-5	2011	UGT1A1 activity correlation analyses using flavonoids-4"-O-glucuronidation vs beta-estradiol-3-glucuronidation (a well-recognized marker for UGT1A1) or vs SN-38 glucuronidation were performed using a bank of HLMs (n = 12) including three UGT1A1-genotyped HLMs (i.e., UGT1A1*1*1, UGT1A1*1*28, and UGT1A1*28*28).	beta-estradiol-3	78-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21840303-2	2011	SN-38 is metabolized to an inactive metabolite SN-38 glucuronide by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-116
21840303-2	2011	SN-38 is metabolized to an inactive metabolite SN-38 glucuronide by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
21840303-2	2011	SN-38 is metabolized to an inactive metabolite SN-38 glucuronide by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1).	7-ethyl-10-hydroxycamptothecin glucuronide	47-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-116
21840303-2	2011	SN-38 is metabolized to an inactive metabolite SN-38 glucuronide by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1).	7-ethyl-10-hydroxycamptothecin glucuronide	47-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
21840303-3	2011	Therefore, single nucleotide polymorphisms (SNPs) of the UGT1A1 gene are responsible for the severe adverse effects associated with the disruption of SN-38 metabolism.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
21840303-4	2011	However, despite having SNPs of the UGT1A1 gene, many patients metabolize SN-38 sufficiently to avoid severe adverse effects.	Irinotecan	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	35-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	70-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
21937736-8	2011	Incubation of raloxifene with human liver microsomes genotyped for UGT1A1*28 showed a significantly reduced metabolic clearance toward M1 in microsomes from donors with *28 allele.	Raloxifene Hydrochloride	14-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
21937736-12	2011	Moreover, the significant influence of UGT1A1*28 polymorphism on metabolism of raloxifene was confirmed.	Raloxifene Hydrochloride	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
21801714-2	2011	Free bilirubin is insoluble; its glucuronidation by bilirubin-UGT enzyme (UGT1A1) makes it soluble and eliminates it through urine and faeces.	Bilirubin	5-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
21997136-8	2011	The EGFR inhibitors increased the S-phase and decreased the UGT1A1 and ABCG expression in irinotecan-resistant cells.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
22333276-0	2011	[Study of irinotecan-induced toxicity and its correlation to UGT1A1 gene promoter polymorphisms].	Irinotecan	10-20	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
22333276-1	2011	OBJECTIVES: To investigate the distribution of uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1) gene promoter polymorphism and its relation to the toxicities caused by irinotecan in Chinese patients with cervical cancer and ovarian cancer.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-94
22333276-1	2011	OBJECTIVES: To investigate the distribution of uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1) gene promoter polymorphism and its relation to the toxicities caused by irinotecan in Chinese patients with cervical cancer and ovarian cancer.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
22333276-5	2011	The relationship between UGT1A1 gene promoter polymorphism and the toxicity caused by irinotecan was analyzed.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
21801714-5	2011	Kinetic study of microsomal UGT1A1 from HepG2 cells suggested that Cln enhanced enzyme activity by increasing V(max) without altering K(m).	carlinoside	67-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
21801714-7	2011	Since Nrf2 is the transcription factor of UGT1A1, we examined whether Cln effect on UGT1A1 overexpression is mediated through Nrf2.	carlinoside	70-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
21801714-2	2011	Free bilirubin is insoluble; its glucuronidation by bilirubin-UGT enzyme (UGT1A1) makes it soluble and eliminates it through urine and faeces.	Bilirubin	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
21801714-10	2011	Results from ChIP assay showed that Cln markedly augmented Nrf2 binding to UGT1A1 promoter that consequently enhanced reporter activity.	carlinoside	36-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
21801714-11	2011	Our findings therefore show that Cln upregulated Nrf2 gene expression, increased its nuclear translocation and stimulated UGT1A1 promoter activity.	carlinoside	33-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
21649640-4	2011	The aim of this study was to determine whether scoparone induces the expression of human UGT1A1.	scoparone	47-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
21740478-0	2011	Genotype-directed, dose-finding study of irinotecan in cancer patients with UGT1A1*28 and/or UGT1A1*6 polymorphisms.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
21933112-6	2011	In particular, the structural basis for regioselective metabolism of flavonoids by SULT1A3 and UGT1A1 is discussed.	Flavonoids	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
21892003-1	2011	Recent findings have disclosed the role of UDP-glucuronosyltransferase (UGT) 1A1*28 on the haematological toxicity induced by irinotecan (CPT-11), a drug commonly used in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-80
21892003-1	2011	Recent findings have disclosed the role of UDP-glucuronosyltransferase (UGT) 1A1*28 on the haematological toxicity induced by irinotecan (CPT-11), a drug commonly used in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	138-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-80
21796020-2	2011	A polymorphic mutation (G71R) of bilirubin UDP-glucuronosyltransferase (UGT1A1) is a known cause of BMJ on the infantile side, but the responsible components of breast milk are not currently known.	(12R)-12-methyltetradecanoic acid	100-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
21796020-3	2011	We analyzed the inhibitory effect of 5beta-pregnane-3alpha,20beta-diol (pregnanediol) on transcriptional activity and enzyme activity of UGT1A1.	5beta-pregnane-3alpha	37-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
21796020-3	2011	We analyzed the inhibitory effect of 5beta-pregnane-3alpha,20beta-diol (pregnanediol) on transcriptional activity and enzyme activity of UGT1A1.	20beta-diol	59-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
21796020-3	2011	We analyzed the inhibitory effect of 5beta-pregnane-3alpha,20beta-diol (pregnanediol) on transcriptional activity and enzyme activity of UGT1A1.	Pregnanediol	72-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
21796020-8	2011	In contrast, in the presence of 100 muM pregnanediol, bilirubin glucuronidation of G71R-UGT1A1 was reduced to 51% of WT.	Pregnanediol	40-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
21796020-8	2011	In contrast, in the presence of 100 muM pregnanediol, bilirubin glucuronidation of G71R-UGT1A1 was reduced to 51% of WT.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
21911884-3	2011	The (GT)n and (TA)n dinucleotide variations in HMOX1 and UGT1A1 gene promoters, respectively, were determined by fragment analysis in all subjects.	Dinucleoside Phosphates	20-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
21740478-0	2011	Genotype-directed, dose-finding study of irinotecan in cancer patients with UGT1A1*28 and/or UGT1A1*6 polymorphisms.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
21740478-1	2011	Irinotecan-induced severe neutropenia is associated with homozygosity for the UGT1A1*28 or UGT1A1*6 alleles.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
21740478-1	2011	Irinotecan-induced severe neutropenia is associated with homozygosity for the UGT1A1*28 or UGT1A1*6 alleles.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
21740478-2	2011	In this study, we determined the maximum-tolerated dose (MTD) of irinotecan in patients with UGT1A1 polymorphisms.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
21740478-14	2011	Patients homozygous for the UGT1A1*28 or UGT1A1*6 allele can receive irinotecan in a starting dose of 150 mg/m(2), but many required dose reductions or delayed treatment in subsequent cycles.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
21740478-14	2011	Patients homozygous for the UGT1A1*28 or UGT1A1*6 allele can receive irinotecan in a starting dose of 150 mg/m(2), but many required dose reductions or delayed treatment in subsequent cycles.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
21524189-5	2011	The potential silybin metabolites were formed in vitro by incubating silybin (i) with the human liver microsomal fraction, (ii) with human hepatocytes and finally (iii) with 12 recombinant UGTs (UGT1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9, 1A10, 2B4, 2B7, 2B15 and 2B17).	Silybin	14-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	195-201
21209233-5	2011	Raltegravir is metabolized primarily by UGT1A1 and is not affected by P450 inhibitors or inducers.	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
21209233-6	2011	Inhibitors of UGT1A1 (eg, atazanavir) can increase plasma concentrations of raltegravir, although this increase has not been found to be clinically meaningful.	Atazanavir Sulfate	26-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
21209233-6	2011	Inhibitors of UGT1A1 (eg, atazanavir) can increase plasma concentrations of raltegravir, although this increase has not been found to be clinically meaningful.	Raltegravir Potassium	76-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
21209233-7	2011	Likewise, inducers of UGT1A1 (eg, rifampin) can reduce plasma concentrations of raltegravir, and the clinical significance of this reduction is being investigated in ongoing clinical studies.	Raltegravir Potassium	80-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
21771946-1	2011	BACKGROUND: Gilbert syndrome, a chronic nonhemolytic unconjugated hyperbilirubinemia, is associated with thymine-adenine (TA) insertions in the UGT1A1 (UDP glucuronosyltransferase 1 family, polypeptide A1) promoter.	thymine-adenine	105-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
21771946-1	2011	BACKGROUND: Gilbert syndrome, a chronic nonhemolytic unconjugated hyperbilirubinemia, is associated with thymine-adenine (TA) insertions in the UGT1A1 (UDP glucuronosyltransferase 1 family, polypeptide A1) promoter.	thymine-adenine	105-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-204
21771946-1	2011	BACKGROUND: Gilbert syndrome, a chronic nonhemolytic unconjugated hyperbilirubinemia, is associated with thymine-adenine (TA) insertions in the UGT1A1 (UDP glucuronosyltransferase 1 family, polypeptide A1) promoter.	Tantalum	122-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
21771946-1	2011	BACKGROUND: Gilbert syndrome, a chronic nonhemolytic unconjugated hyperbilirubinemia, is associated with thymine-adenine (TA) insertions in the UGT1A1 (UDP glucuronosyltransferase 1 family, polypeptide A1) promoter.	Tantalum	122-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-204
21771946-2	2011	The UGT1A1 promoter genotype also correlates with toxicity induced by the chemotherapeutic drug irinotecan.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
22866151-0	2011	Prevalence of topoisomerase I genetic mutations and UGT1A1 polymorphisms associated with irinotecan in individuals of Asian descent.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
22866151-3	2011	On the other hand, polymorphisms of UGT1A1 have been shown to be associated with CPT-11 toxicity in clinical situations.	Irinotecan	81-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
21829131-8	2011	Metabolic clearance of telmisartan in human liver microsomes obtained from individuals with UGT1A1*28/*28 was higher compared with that of UGT1A1*1/*1 (168+-33 vs. 93.3+-27.3 mul/min/mg protein).	Telmisartan	23-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
21555506-12	2011	Summing up, we showed that, whereas liver P450 isoenzymes were involved in the metabolism of C-1311 to a limited extent, FMO plays a significant role in the microsomal transformations of this compound, which is also a specific substrate of UGT1A1.	C 1311	93-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	240-246
21826053-3	2011	Corydaline also demonstrated moderate inhibition of UGT1A1-mediated 17b-estradiol 3-glucuronidation and UGT1A9-mediated propofol glucuronidation with K(i) values of 57.6 and 37.3 mM, respectively.	corydaline	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
21826053-3	2011	Corydaline also demonstrated moderate inhibition of UGT1A1-mediated 17b-estradiol 3-glucuronidation and UGT1A9-mediated propofol glucuronidation with K(i) values of 57.6 and 37.3 mM, respectively.	Estradiol	68-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
21624356-0	2011	Simple and precise detection of UGT1A1 polymorphisms with a modified loop-hybrid mobility shift assay using Cy5-labeled loop probes.	cyanine dye 5	108-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
21636218-1	2011	Patients with Gilbert syndrome have an impaired function of the enzyme UGT1A1, responsible for the degradation of 4-OH-estrogens.	4-oh	114-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
21585235-6	2011	This achievement has led to personalized irinotecan therapy, reflecting ethnic differences in UGT1A1 genotypes, and possible benefits of genetic testing have also been suggested for gemcitabine and tamoxifen therapy, which still requires further validation.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
21472492-2	2011	We aimed to determine the regioselective glucuronidation of four model flavonols using six expressed human UGT1A isoforms (UGT1A1, 1A3, 1A7, 1A8, 1A9, 1A10).	Flavonols	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
21472492-4	2011	RESULTS: UGT1A1 and 1A3 regioselectively metabolized the 7-OH group, whereas UGT1A7, 1A8, 1A9 and 1A10 preferred to glucuronidate the 3-OH group.	7-oh	57-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
21472492-4	2011	RESULTS: UGT1A1 and 1A3 regioselectively metabolized the 7-OH group, whereas UGT1A7, 1A8, 1A9 and 1A10 preferred to glucuronidate the 3-OH group.	3-oh	134-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
21413806-4	2011	UGT 1A1 equally glucuronidated 3-O (glucuronic acid substituted at C-3 hydroxyl group), 7-O, and 4"-O, whereas UGTs 1A8 and 1A9 preferably glucuronidated only 3-O and 7-O positions.	3-o	31-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-7
22169899-1	2011	The UGT1A1 gene encodes a responsible enzyme, UDP-glucuronosyltransferase1A1, for bilirubin metabolism.	Bilirubin	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
22169899-1	2011	The UGT1A1 gene encodes a responsible enzyme, UDP-glucuronosyltransferase1A1, for bilirubin metabolism.	Bilirubin	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-76
21287524-2	2011	The UGT1A1 gene encodes for an enzyme that metabolizes irinotecan, and its genetic variants were shown to be associated with increased drug toxicity.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
21287524-12	2011	CONCLUSIONS: The UGT1A1*28 7/7 genotype is strongly associated with severe hematological toxicity and higher hospitalization rate and predicts lower survival of colorectal cancer in users of irinotecan.	Irinotecan	191-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
21413806-4	2011	UGT 1A1 equally glucuronidated 3-O (glucuronic acid substituted at C-3 hydroxyl group), 7-O, and 4"-O, whereas UGTs 1A8 and 1A9 preferably glucuronidated only 3-O and 7-O positions.	Glucuronic Acid	36-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-7
21654688-2	2011	Irinotecan is converted into 7-ethyl-10-hydroxycamptothecin (SN-38) by a carboxylsterase and metabolised through uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
21412181-2	2011	Two patients during clinical development met laboratory, but not clinical, criteria for Hy"s law with bilirubin elevations suspected as a result of genetic variation in uridine diphosphoglucose glucuronosyltransferase (UGT1A1) typical of Gilbert syndrome.	Bilirubin	102-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	219-225
21412181-7	2011	UGT1A1*28 and three additional single nucleotide polymorphisms showed odds ratios greater than 25 for associations with elevated bilirubin.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21412181-10	2011	Thus, in the absence of other signs of hepatic dysfunction, bilirubin elevations after treatment with tocilizumab have a high probability of association with UGT1A1 polymorphism, which should alleviate concerns of serious hepatotoxicity.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
21507987-9	2011	Regulation of UGT1A1 and UGT1A9 expression showed that the induction of DNA adducts by BaP is directly affected by their expression levels.	Benzo(a)pyrene	87-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
21654688-2	2011	Irinotecan is converted into 7-ethyl-10-hydroxycamptothecin (SN-38) by a carboxylsterase and metabolised through uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	29-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
21654688-2	2011	Irinotecan is converted into 7-ethyl-10-hydroxycamptothecin (SN-38) by a carboxylsterase and metabolised through uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
21466813-12	2011	Resveratrol at its IC(50) mediated a four-fold induction of UGT1A1 mRNA in a concentration independent manner.	Resveratrol	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
21317830-0	2011	Association of the UGT1A1-53(TA)n polymorphism with L-thyroxine doses required for thyrotropin suppression in patients with differentiated thyroid cancer.	Thyroxine	52-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
21235620-8	2011	Dasatinib and imatinib also inhibited UGT1A1-mediated paracetamol glucuronidation.	Dasatinib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
21235620-8	2011	Dasatinib and imatinib also inhibited UGT1A1-mediated paracetamol glucuronidation.	Imatinib Mesylate	14-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
21235620-8	2011	Dasatinib and imatinib also inhibited UGT1A1-mediated paracetamol glucuronidation.	Acetaminophen	54-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
21317540-4	2011	When UGT1A-expressing HEK293 cells and LS180 cells were treated with curcumin or calphostin C, the exogenous and endogenous UGT1A protein levels in homogenates prepared with Tris-buffered saline were significantly decreased.	Curcumin	69-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-10
21317540-4	2011	When UGT1A-expressing HEK293 cells and LS180 cells were treated with curcumin or calphostin C, the exogenous and endogenous UGT1A protein levels in homogenates prepared with Tris-buffered saline were significantly decreased.	Curcumin	69-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-129
21317540-4	2011	When UGT1A-expressing HEK293 cells and LS180 cells were treated with curcumin or calphostin C, the exogenous and endogenous UGT1A protein levels in homogenates prepared with Tris-buffered saline were significantly decreased.	calphostin C	81-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-10
21317540-4	2011	When UGT1A-expressing HEK293 cells and LS180 cells were treated with curcumin or calphostin C, the exogenous and endogenous UGT1A protein levels in homogenates prepared with Tris-buffered saline were significantly decreased.	tris-buffered saline	174-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-129
20852006-2	2011	A prior investigation of raltegravir coadministered with rifampin demonstrated a decrease in plasma concentrations of raltegravir likely secondary to induction of UGT1A1, the enzyme primarily responsible for the metabolism of raltegravir.	Raltegravir Potassium	25-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
20852006-2	2011	A prior investigation of raltegravir coadministered with rifampin demonstrated a decrease in plasma concentrations of raltegravir likely secondary to induction of UGT1A1, the enzyme primarily responsible for the metabolism of raltegravir.	Rifampin	57-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
20852006-2	2011	A prior investigation of raltegravir coadministered with rifampin demonstrated a decrease in plasma concentrations of raltegravir likely secondary to induction of UGT1A1, the enzyme primarily responsible for the metabolism of raltegravir.	Raltegravir Potassium	118-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
20852006-2	2011	A prior investigation of raltegravir coadministered with rifampin demonstrated a decrease in plasma concentrations of raltegravir likely secondary to induction of UGT1A1, the enzyme primarily responsible for the metabolism of raltegravir.	Raltegravir Potassium	118-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
20852006-3	2011	Little is known regarding the induction of UGT1A1 by rifabutin, an alternate rifamycin.	Rifabutin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
20852006-5	2011	In vitro studies indicate that rifabutin is a less potent inducer of UGT1A1 messenger RNA expression than is rifampin.	Rifabutin	31-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
21466813-0	2011	Resveratrol in combination with other dietary polyphenols concomitantly enhances antiproliferation and UGT1A1 induction in Caco-2 cells.	Resveratrol	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
21466813-0	2011	Resveratrol in combination with other dietary polyphenols concomitantly enhances antiproliferation and UGT1A1 induction in Caco-2 cells.	Polyphenols	46-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
21317830-4	2011	These results are consistent with reduced T4 glucuronidation in patients with low-expression (TA)7 and (TA)8 alleles and provide the first evidence for association between UGT1A1-53(TA)n and T4-dose requirement for thyroid-stimulating hormone suppression in a natural clinical setting.	Thyrotropin	215-242	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	172-178
21245288-5	2011	Higher NFA concentrations (50-100 muM) inhibited UGT1A1 and UGT2B15 but had little effect on the activities of UGT1A3, UGT1A4, UGT1A6, UGT2B4, UGT2B7, and UGT2B17.	Niflumic Acid	7-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
21417257-2	2011	The present study investigated the phase II metabolism of feruloylquinic acids with selected human sulfotransferases (SULT1A1 and SULT1E1) and uridine 5"-diphosphoglucuronosyltransferases (UGT1A1 and UGT1A9).	1,3-di-O-feruloylquinic acid	58-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
21266593-2	2011	The development of UGT1A1 and 1A6 was studied in 50 pediatric liver samples using bilirubin, serotonin activity assays, and Western blot as well as pharmacokinetic scaling.	Bilirubin	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-33
21266593-2	2011	The development of UGT1A1 and 1A6 was studied in 50 pediatric liver samples using bilirubin, serotonin activity assays, and Western blot as well as pharmacokinetic scaling.	Serotonin	93-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-33
21538282-5	2011	Linkage and case-control studies of candidate genes and recent genome-wide studies have identified multiple lithogenic genes, in particular the hepatocanalicular cholesterol transporter ABCG5/G8 and the bilirubin conjugating enzyme UGT1A1, as major genetic determinants of gallstones in humans.	Bilirubin	203-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	232-238
21353662-7	2011	Variants of the gene encoding UGT1A1 (uridine 5"-diphosphate (UDP)-glucuronosyltransferase 1A1) responsible for bilirubin conjugation were recently associated with risk of gallstones as well as stone bilirubin content, suggesting common factors in cholesterol and pigment gallstone pathogenesis.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
21353662-7	2011	Variants of the gene encoding UGT1A1 (uridine 5"-diphosphate (UDP)-glucuronosyltransferase 1A1) responsible for bilirubin conjugation were recently associated with risk of gallstones as well as stone bilirubin content, suggesting common factors in cholesterol and pigment gallstone pathogenesis.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-94
21353662-7	2011	Variants of the gene encoding UGT1A1 (uridine 5"-diphosphate (UDP)-glucuronosyltransferase 1A1) responsible for bilirubin conjugation were recently associated with risk of gallstones as well as stone bilirubin content, suggesting common factors in cholesterol and pigment gallstone pathogenesis.	Bilirubin	200-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
21353662-7	2011	Variants of the gene encoding UGT1A1 (uridine 5"-diphosphate (UDP)-glucuronosyltransferase 1A1) responsible for bilirubin conjugation were recently associated with risk of gallstones as well as stone bilirubin content, suggesting common factors in cholesterol and pigment gallstone pathogenesis.	Bilirubin	200-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-94
21353662-7	2011	Variants of the gene encoding UGT1A1 (uridine 5"-diphosphate (UDP)-glucuronosyltransferase 1A1) responsible for bilirubin conjugation were recently associated with risk of gallstones as well as stone bilirubin content, suggesting common factors in cholesterol and pigment gallstone pathogenesis.	Cholesterol	248-259	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
21353662-7	2011	Variants of the gene encoding UGT1A1 (uridine 5"-diphosphate (UDP)-glucuronosyltransferase 1A1) responsible for bilirubin conjugation were recently associated with risk of gallstones as well as stone bilirubin content, suggesting common factors in cholesterol and pigment gallstone pathogenesis.	Cholesterol	248-259	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-94
21368751-3	2011	We have shown in vitro that ezetimibe and tacrolimus may interact in competition for intestinal UGT1A1 and ABCB1 at concentrations reached in gut lumen after oral administration.	Ezetimibe	28-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
21368751-3	2011	We have shown in vitro that ezetimibe and tacrolimus may interact in competition for intestinal UGT1A1 and ABCB1 at concentrations reached in gut lumen after oral administration.	Tacrolimus	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
21346002-3	2011	T-5224 was converted to its acyl O-glucuronide (G2) by UGT1A1 and UGT1A3 and to its hydroxyl O-glucuronide (G3) by several UGTs, but it was not metabolized by the P450s.	3-(5-(4-(cyclopentyloxy)-2-hydroxybenzoyl)-2-((3-hydroxy-1,2-benzisoxazol-6-yl)methoxy)phenyl)propionic acid	0-6	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
21346002-6	2011	A high correlation was observed between G2 formation activity and UGT1A1-specific activity (beta-estradiol 3-glucuronidation) in seven individual HLM.	Estradiol	92-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
21513526-2	2011	Previous genetic studies have focused on the UGT1A1 gene, associating common variation in the coding or promoter regions with qualitative assessments of bilirubin (i.e. significantly elevated or not).	Bilirubin	153-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
21513526-5	2011	We apply this approach to the UGT1A1 gene--exploring the contribution of both rare and common variants to early bilirubin changes.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
21513526-9	2011	CONCLUSIONS: Collectively, rare UGT1A1 coding variants do not appear to play a prominent role in determining early bilirubin levels; however common variants in the 3" UTR of UGT1A1 may modulate the early bilirubin rise.	Bilirubin	204-213	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
21189330-9	2011	We conclude that limited in vivo metabolism of AR-67 by UGT1A1 may partly explain the absence of AR-67 glucuronides in plasma and hypothesize that UGT1A8- and CYP3A-mediated biotransformation within the gastrointestinal epithelium may provide protective mechanisms against AR-67 gastrointestinal toxicity.	Argon	47-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
21245288-9	2011	Consistent with previous reports, APAP was glucuronidated by recombinant UGT1A1, UGT1A6, UGT1A9, and UGT2B15.	Acetaminophen	34-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
21245288-10	2011	NFA concentrations in the range of 2.5 to 100 muM inhibited APAP glucuronidation by UGT1A1, UGT1A9, and UGT2B15 but not by UGT1A6.	Niflumic Acid	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
21216137-2	2011	In vitro studies have shown that omeprazole can alter the function of metabolic enzymes and transporters that are involved in the metabolism of irinotecan, such as uridine diphosphate glucuronosyltransferase subfamily 1A1 (UGT1A1), cytochrome P-450 enzymes subfamily 3A (CYP3A) and ATP-binding cassette drug-transporter G2 (ABCG2).	Omeprazole	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	223-229
21255081-6	2011	Bilirubin concentrations were significantly higher among individuals with compound heterozygous variations/homozygous variation in the UGT1A1 gene than in those possessing the wild type and heterozygous variation (P &lt; 0.001 for both alpha- and beta-thalassemia heterozygotes).	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
21255081-8	2011	CONCLUSIONS:   The difference in bilirubin concentrations between alpha- and beta-thalassemia heterozygotes may be attributable to more bilirubin being produced in beta-thalassemia heterozygotes than in alpha-thalassemia heterozygotes, while variation status of the UGT1A1 gene affects bilirubin concentrations in both alpha- and beta-thalassemia heterozygotes.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	266-272
21216137-2	2011	In vitro studies have shown that omeprazole can alter the function of metabolic enzymes and transporters that are involved in the metabolism of irinotecan, such as uridine diphosphate glucuronosyltransferase subfamily 1A1 (UGT1A1), cytochrome P-450 enzymes subfamily 3A (CYP3A) and ATP-binding cassette drug-transporter G2 (ABCG2).	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	223-229
21255081-8	2011	CONCLUSIONS:   The difference in bilirubin concentrations between alpha- and beta-thalassemia heterozygotes may be attributable to more bilirubin being produced in beta-thalassemia heterozygotes than in alpha-thalassemia heterozygotes, while variation status of the UGT1A1 gene affects bilirubin concentrations in both alpha- and beta-thalassemia heterozygotes.	Bilirubin	136-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	266-272
21255081-8	2011	CONCLUSIONS:   The difference in bilirubin concentrations between alpha- and beta-thalassemia heterozygotes may be attributable to more bilirubin being produced in beta-thalassemia heterozygotes than in alpha-thalassemia heterozygotes, while variation status of the UGT1A1 gene affects bilirubin concentrations in both alpha- and beta-thalassemia heterozygotes.	Bilirubin	136-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	266-272
21411679-0	2011	Serum bilirubin links UGT1A1*28 polymorphism and predicts long-term cardiovascular events and mortality in chronic hemodialysis patients.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
21366639-4	2011	SN-38 is subsequently detoxified by uridine diphosphate-glycosyltransferase 1, encoded by the UGT1A1 gene.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
22214020-0	2011	[Treatment with CPT-11 based on the UGT1A1 genetic polymorphism].	Irinotecan	16-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
21309756-1	2011	Variation of a short (TA)(n) repeat sequence (rs8175347) covering the TATA box of UGT1A1 (UDP-glucuronosyltransferase1A1) is associated with hyperbilirubinaemia (Gilbert"s syndrome) and adverse drug reactions, and is used for dosage advice for irinotecan.	Irinotecan	244-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
21309756-1	2011	Variation of a short (TA)(n) repeat sequence (rs8175347) covering the TATA box of UGT1A1 (UDP-glucuronosyltransferase1A1) is associated with hyperbilirubinaemia (Gilbert"s syndrome) and adverse drug reactions, and is used for dosage advice for irinotecan.	Irinotecan	244-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-120
21242184-3	2011	Although she achieved long-term survival of more than 2 years, the last-line chemotherapy, consisting of irinotecan, induced grade 4 febrile neutropenia and her performance status deteriorated even with a reduced dose according to the analysis of UDP-glucuronosyltransferase 1A1.	Irinotecan	105-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	247-278
21411679-2	2011	Bilirubin degradation is mainly determined by the activity of hepatic bilirubin uridine diphosphate-glucuronosyltransferase (UGT1A1), which is significantly influenced by a TA-repeat polymorphism in the gene"s promoter, an allele designated UGT1A1*28.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
21411679-2	2011	Bilirubin degradation is mainly determined by the activity of hepatic bilirubin uridine diphosphate-glucuronosyltransferase (UGT1A1), which is significantly influenced by a TA-repeat polymorphism in the gene"s promoter, an allele designated UGT1A1*28.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	241-247
21411679-3	2011	The study aimed to clarify the association between serum bilirubin and UGT1A1*28 polymorphism and their respective effect on outcomes of chronic hemodialysis patients.	Bilirubin	57-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
21411679-7	2011	Individuals homozygous for UGT1A1*28 (genotype 7/7) had significantly higher bilirubin levels than those with 6/6 and 7/6 genotypes.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
21411679-10	2011	Moreover, the UGT1A1*28 polymorphism had strong effects on bilirubin levels and the 7/7 genotype might have an important effect on reducing CVEs and death.	Bilirubin	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
21980965-3	2011	Her HIV treatment was switched to raltegravir which is metabolized by UGT1A1 which does not affect tacrolimus.	Raltegravir Potassium	34-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
21123165-4	2011	Glucuronidation of MPA, as well as the expression and probe substrate activity of UGTs primarily responsible for MPA phenol glucuronide (MPAG) formation (UGT1A1 and UGT1A9), and MPA acyl glucuronide (AcMPAG) formation (UGT2B7), was characterized.	mycophenolic acid glucuronide	137-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
20177420-2	2011	Irinotecan"s active metabolite is inactivated by UDP-glucuronosyltransferase 1A1 (UGT1A1), which is deficient in Gilbert"s syndrome.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-80
20177420-2	2011	Irinotecan"s active metabolite is inactivated by UDP-glucuronosyltransferase 1A1 (UGT1A1), which is deficient in Gilbert"s syndrome.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
21297369-4	2011	Irinotecan, now used for treatments of many cancers, is metabolically activated to SN-38 and then inactivated to SN-38 glucuronide by a UDP-glucuronosyltransferase UGT1A1.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
21297369-4	2011	Irinotecan, now used for treatments of many cancers, is metabolically activated to SN-38 and then inactivated to SN-38 glucuronide by a UDP-glucuronosyltransferase UGT1A1.	7-ethyl-10-hydroxycamptothecin glucuronide	113-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
21080475-3	2011	Genetic variation within the promoter region of uridine diphosphate glucuronosyltransferase (UGT1A1) on chromosome 2q has been associated with elevated serum bilirubin levels in European populations.	Bilirubin	158-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
21080475-10	2011	CONCLUSIONS: Replication of a serum bilirubin QTL on chromosome 2q in American Indians implicates UGT1A1 but further genotyping is warranted to identify additional causative polymorphisms.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
23461146-1	2011	The UDP-glucuronosyltransferase 1A1 gene that encode the enzyme UGT1A1 responsible for glucuronidation undergoes several variations that may affect the enzymatic activity or expression and which are the cause of metabolic disorders related to the glucuronidation of bilirubin, such as Gilbert"s syndrome and Crigler Najjar"s syndrome.	Bilirubin	266-275	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-35
23461146-1	2011	The UDP-glucuronosyltransferase 1A1 gene that encode the enzyme UGT1A1 responsible for glucuronidation undergoes several variations that may affect the enzymatic activity or expression and which are the cause of metabolic disorders related to the glucuronidation of bilirubin, such as Gilbert"s syndrome and Crigler Najjar"s syndrome.	Bilirubin	266-275	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
22135857-2	2011	The causative mutation in Caucasians is almost exclusively a (TA) dinucleotide insertion in the UGT1A1 promoter.	(ta) dinucleotide	61-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
22135857-10	2011	CONCLUSIONS: We developed a new DHPLC assay which is suitable for accurate, automated, highthroughput, robust genotyping of all UGT1A1(TA)n polymorphism variants, compared to a labour intensive and time-consuming SSCP assay.	dhplc	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
20680278-8	2011	CONCLUSIONS: Additional in vitro experiments suggest that these results can be explained by induction of UGT1A1 by methimazole, leading to higher SN-38G concentrations.	Methimazole	115-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
20680278-8	2011	CONCLUSIONS: Additional in vitro experiments suggest that these results can be explained by induction of UGT1A1 by methimazole, leading to higher SN-38G concentrations.	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
20814789-0	2011	The small-molecule tyrosine kinase inhibitor nilotinib is a potent noncompetitive inhibitor of the SN-38 glucuronidation by human UGT1A1.	nilotinib	45-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
20814789-0	2011	The small-molecule tyrosine kinase inhibitor nilotinib is a potent noncompetitive inhibitor of the SN-38 glucuronidation by human UGT1A1.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
20814789-1	2011	PURPOSE: Inhibition of the UDP-glucuronosyltransferase (UGT) 1A1 by nilotinib was examined in vitro with SN-38 as a substrate, to estimate the possibility of drug-drug interaction of nilotinib with other medicines predominantly detoxified by UGT1A1.	nilotinib	68-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-64
20814789-1	2011	PURPOSE: Inhibition of the UDP-glucuronosyltransferase (UGT) 1A1 by nilotinib was examined in vitro with SN-38 as a substrate, to estimate the possibility of drug-drug interaction of nilotinib with other medicines predominantly detoxified by UGT1A1.	nilotinib	68-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	242-248
20814789-1	2011	PURPOSE: Inhibition of the UDP-glucuronosyltransferase (UGT) 1A1 by nilotinib was examined in vitro with SN-38 as a substrate, to estimate the possibility of drug-drug interaction of nilotinib with other medicines predominantly detoxified by UGT1A1.	Irinotecan	105-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-64
20814789-2	2011	METHODS: Inhibition of UGT1A1-catalyzed SN-38 glucuronidation by nilotinib was examined with human liver microsomes (HLM) and recombinant human UGT1A1 as enzyme sources.	Irinotecan	40-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
20814789-2	2011	METHODS: Inhibition of UGT1A1-catalyzed SN-38 glucuronidation by nilotinib was examined with human liver microsomes (HLM) and recombinant human UGT1A1 as enzyme sources.	nilotinib	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
20814789-2	2011	METHODS: Inhibition of UGT1A1-catalyzed SN-38 glucuronidation by nilotinib was examined with human liver microsomes (HLM) and recombinant human UGT1A1 as enzyme sources.	nilotinib	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
20814789-4	2011	RESULTS: Nilotinib potently inhibited the SN-38 glucuronidation by human liver microsomal UGT1A1 and recombinant UGT1A1 in a noncompetitive manner, with K(i) values of 0.286 +- 0.0094 and 0.079 +- 0.0029 muM, respectively.	nilotinib	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
20814789-4	2011	RESULTS: Nilotinib potently inhibited the SN-38 glucuronidation by human liver microsomal UGT1A1 and recombinant UGT1A1 in a noncompetitive manner, with K(i) values of 0.286 +- 0.0094 and 0.079 +- 0.0029 muM, respectively.	nilotinib	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
20814789-4	2011	RESULTS: Nilotinib potently inhibited the SN-38 glucuronidation by human liver microsomal UGT1A1 and recombinant UGT1A1 in a noncompetitive manner, with K(i) values of 0.286 +- 0.0094 and 0.079 +- 0.0029 muM, respectively.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
20814789-4	2011	RESULTS: Nilotinib potently inhibited the SN-38 glucuronidation by human liver microsomal UGT1A1 and recombinant UGT1A1 in a noncompetitive manner, with K(i) values of 0.286 +- 0.0094 and 0.079 +- 0.0029 muM, respectively.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
20814789-5	2011	If a drug that serves as a substrate of UGT1A1 is administered with nilotinib, the area under the plasma concentration-time curve of a drug estimated by using these K(i) values would be two times or higher than that without nilotinib, suggesting drug-drug interactions involving UGT1A1.	nilotinib	68-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
20814789-5	2011	If a drug that serves as a substrate of UGT1A1 is administered with nilotinib, the area under the plasma concentration-time curve of a drug estimated by using these K(i) values would be two times or higher than that without nilotinib, suggesting drug-drug interactions involving UGT1A1.	nilotinib	68-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	279-285
20814789-5	2011	If a drug that serves as a substrate of UGT1A1 is administered with nilotinib, the area under the plasma concentration-time curve of a drug estimated by using these K(i) values would be two times or higher than that without nilotinib, suggesting drug-drug interactions involving UGT1A1.	nilotinib	224-233	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
20814789-7	2011	CONCLUSION: We found that nilotinib is a potent noncompetitive inhibitor of human UGT1A1 activity.	nilotinib	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
21673874-11	2011	The hyperbilirubinemia seen in both groups may be at least partly related to inhibition of UGT1A1 by sorafenib.	Sorafenib	101-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
21468552-4	2011	UDP-glucuronosyltransferase (UGT)1A1 is a conjugating biotransformation enzyme that plays a role in maintaining the levels of endogenous compounds (e.g., bilirubin) and in handling exogenous compounds, including carcinogens.	Bilirubin	154-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-36
21468552-5	2011	It has been demonstrated that the UGT1A1*28 polymorphism plays a predictive role in patients administered an irinotecan-containing regimen.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	182-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	182-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
21030469-0	2011	Correlation between bilirubin glucuronidation and estradiol-3-gluronidation in the presence of model UDP-glucuronosyltransferase 1A1 substrates/inhibitors.	Bilirubin	20-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-132
21030469-1	2011	Inhibition of UDP-glucuronosyltransferase (UGT) 1A1-catalyzed bilirubin glucuronidation by drug compounds may potentially be of clinical concern.	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-51
21030469-5	2011	The glucuronidation kinetics of bilirubin and estradiol were carefully characterized with recombinant UGT1A1 expressed in human embryonic kidney 293 cells.	Bilirubin	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
21030469-11	2011	In addition, 7-ethyl-10-hydroxycamptothecin, a substrate of UGT1A1 (reported K(m) = 24 muM) seemed to be a weak inhibitor of bilirubin glucuronidation (IC(50) = 356.4 muM) but a partial inhibitor of estradiol-3-glucuronidation.	Irinotecan	13-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
21030469-11	2011	In addition, 7-ethyl-10-hydroxycamptothecin, a substrate of UGT1A1 (reported K(m) = 24 muM) seemed to be a weak inhibitor of bilirubin glucuronidation (IC(50) = 356.4 muM) but a partial inhibitor of estradiol-3-glucuronidation.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
21030469-11	2011	In addition, 7-ethyl-10-hydroxycamptothecin, a substrate of UGT1A1 (reported K(m) = 24 muM) seemed to be a weak inhibitor of bilirubin glucuronidation (IC(50) = 356.4 muM) but a partial inhibitor of estradiol-3-glucuronidation.	Estradiol	199-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
21614935-1	2011	Bilirubin is glucoronized by uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1) mainly in the liver, and excreted into bile.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-77
21614935-1	2011	Bilirubin is glucoronized by uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1) mainly in the liver, and excreted into bile.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
20975617-7	2011	Neonates with nucleotide 211 GA or AA variation in UGT1A1 genotypes had higher peak serum bilirubin levels and higher incidence of hyperbilirubinemia than WTs (GG).	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
20854796-2	2011	A microarrays analysis between sensitive and methotrexate resistant MCF7 and MDA-MB-468 breast cancer cells pointed out the UDP-glucuronosyltransferase 1A (UGT1A) family as a common deregulated node in both cell lines.	Methotrexate	45-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-154
20854796-2	2011	A microarrays analysis between sensitive and methotrexate resistant MCF7 and MDA-MB-468 breast cancer cells pointed out the UDP-glucuronosyltransferase 1A (UGT1A) family as a common deregulated node in both cell lines.	Methotrexate	45-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-161
22110515-0	2011	Is Ceftriaxone-Induced Biliary Pseudolithiasis Influenced by UDP-Glucuronosyltransferase 1A1 Gene Polymorphisms?	Ceftriaxone	3-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-92
22110515-3	2011	We describe 3 children with ceftriaxone-induced pseudolithiasis, who were also carriers of the A(TA)(7)TAA polymorphism of the UGT1A1 gene, implying that a cause and effect relation may exist.	Ceftriaxone	28-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
21422672-11	2011	Moreover, octyl gallate, a marker substrate of UGT1A1, competitively inhibited FA glucuronidation mediated by this isoform.	octyl gallate	10-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
20926993-1	2010	Raltegravir (RAL) is primarily metabolized by uridine diphosphate-glucorunosyl transferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-94
20865252-2	2011	Ezetimibe is readily absorbed, and undergoes rapid and almost complete glucuronidation by UGT, particularly UGT1A1, in enterocytes during its first pass.	Ezetimibe	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
20528568-6	2011	RESULTS: The UGT1A1*28 polymorphism was associated with total cholesterol (T-chol) (p = 0.030; corrected p = 0.060) and low-density lipoprotein cholesterol (LDL-C) levels (p = 0.011, corrected p = 0.022) in premenopausal women.	Cholesterol	62-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
20528568-6	2011	RESULTS: The UGT1A1*28 polymorphism was associated with total cholesterol (T-chol) (p = 0.030; corrected p = 0.060) and low-density lipoprotein cholesterol (LDL-C) levels (p = 0.011, corrected p = 0.022) in premenopausal women.	t-chol	75-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
20528568-8	2011	CONCLUSION: The data showed the presence of an association between the UGT1A1*28/*28 and SULT1A1*2/*2 and T-chol and LDL-C levels in women with different hormonal status.	chol	108-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
20648548-0	2011	Selective regulation of UGT1A1 and SREBP-1c mRNA expression by docosahexaenoic, eicosapentaenoic, and arachidonic acids.	docosahexaenoic	63-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
20648548-0	2011	Selective regulation of UGT1A1 and SREBP-1c mRNA expression by docosahexaenoic, eicosapentaenoic, and arachidonic acids.	eicosapentaenoic	80-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
20648548-0	2011	Selective regulation of UGT1A1 and SREBP-1c mRNA expression by docosahexaenoic, eicosapentaenoic, and arachidonic acids.	Arachidonic Acids	102-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
20648548-8	2011	Nevertheless, when these PUFAs were combined with Vit.E, which by itself did not produce any effect, the result was a reduction of UGT1A1 mRNA with DHA, an increase reverting to basal level with EPA and no variation with AA.	dehydroacetic acid	148-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
21351260-1	2010	UDP-glucuronosyltransferase 1A1 (UGT1A1) is an enzyme which catalyses not only the glucuronidation of tobacco smoke carcinogens like benzopyrene, but also of the endogenous substrate bilirubin.	Benzopyrenes	133-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
21351260-1	2010	UDP-glucuronosyltransferase 1A1 (UGT1A1) is an enzyme which catalyses not only the glucuronidation of tobacco smoke carcinogens like benzopyrene, but also of the endogenous substrate bilirubin.	Bilirubin	183-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
21351260-8	2010	In conclusion, the predicted high activity UGT1A1*1 polymorphism, which results in lower serum levels of the endogenous antioxidant bilirubin, was associated with an increased risk of head and neck cancer.	Bilirubin	132-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
21191764-5	2010	Jaceosidin glucuronidation was catalyzed by UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9, and UGT1A10.	jaceosidin glucuronidation	0-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
21191764-6	2010	These results suggest that the pharmacokinetics of jaceosidin may be dramatically affected by polymorphic CYP1A2, UGT1A1, and UGT1A7 responsible for the metabolism of jaceosidin or by the coadministration of relevant CYP1A2 or UGT inhibitors or inducers.	jaceosidin	51-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
21191764-6	2010	These results suggest that the pharmacokinetics of jaceosidin may be dramatically affected by polymorphic CYP1A2, UGT1A1, and UGT1A7 responsible for the metabolism of jaceosidin or by the coadministration of relevant CYP1A2 or UGT inhibitors or inducers.	jaceosidin	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
21150467-13	2011	The UGT1A1*6 and UGT1A1*27 genotypes might be useful predictors of grade 4 neutropenia in patients who receive irinotecan-based chemotherapy.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
21150467-13	2011	The UGT1A1*6 and UGT1A1*27 genotypes might be useful predictors of grade 4 neutropenia in patients who receive irinotecan-based chemotherapy.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
21175442-4	2010	Finally, a panel of human liver microsomes (genotyped for UGT1A1*28 allele status) was used to determine the importance of UGT1A1 in the direct glucuronidation of repaglinide.	repaglinide	163-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
21175442-10	2010	UGT1A1 plays a significant role in the glucuronidation of repaglinide.	repaglinide	58-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Gemfibrozil	62-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Glucuronides	82-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	repaglinide	176-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Gemfibrozil	192-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
20837016-5	2010	RESULTS: By using the presence of bilirubin as a phenotype, variants rs6742078 (UGT1A1; P = .003), rs4149056 (SLCO1B1; P = .003), and rs4149000 (SLCO1A2; P = .015) were associated with gallstone composition.	Bilirubin	34-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
20837016-10	2010	CONCLUSIONS: The UGT1A1 Gilbert syndrome variant rs6742078 is associated with gallstone disease in men; further studies are required regarding the sex-specific physiology of bilirubin and bile acid metabolism.	Bilirubin	174-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
20837016-10	2010	CONCLUSIONS: The UGT1A1 Gilbert syndrome variant rs6742078 is associated with gallstone disease in men; further studies are required regarding the sex-specific physiology of bilirubin and bile acid metabolism.	Bile Acids and Salts	188-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
21284263-1	2010	The aim of the present study was to investigate the inhibitory effects of medroxyprogesterone acetate (MPA) on four important UGT isoforms (UGT1A1, 1A6, 1A9 and 2B7).	Medroxyprogesterone Acetate	74-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
21284263-1	2010	The aim of the present study was to investigate the inhibitory effects of medroxyprogesterone acetate (MPA) on four important UGT isoforms (UGT1A1, 1A6, 1A9 and 2B7).	Medroxyprogesterone Acetate	103-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
20926993-1	2010	Raltegravir (RAL) is primarily metabolized by uridine diphosphate-glucorunosyl transferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
20926993-2	2010	Atazanavir (ATV), a strong inhibitor of UGT1A1, has been shown to increase plasma concentrations of RAL by approximately 50% in healthy volunteers.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
20926993-2	2010	Atazanavir (ATV), a strong inhibitor of UGT1A1, has been shown to increase plasma concentrations of RAL by approximately 50% in healthy volunteers.	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
20926993-8	2010	Notably, patients with ATV AUC 0-12 above the mean or with concentrations exceeding the half maximal inhibitory concentration for UGT1A1 had twofold higher RAL AUCs compared with patients with lower ATV exposure.	Atazanavir Sulfate	23-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
20926993-8	2010	Notably, patients with ATV AUC 0-12 above the mean or with concentrations exceeding the half maximal inhibitory concentration for UGT1A1 had twofold higher RAL AUCs compared with patients with lower ATV exposure.	Atazanavir Sulfate	199-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
20823282-1	2010	Atazanavir inhibits UDP-glucuronyl-transferase-1A1 (UGT1A1), which metabolizes raltegravir, but the magnitude of steady-state inhibition and role of the UGT1A1 genotype are unknown.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-50
20823282-1	2010	Atazanavir inhibits UDP-glucuronyl-transferase-1A1 (UGT1A1), which metabolizes raltegravir, but the magnitude of steady-state inhibition and role of the UGT1A1 genotype are unknown.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
20823282-1	2010	Atazanavir inhibits UDP-glucuronyl-transferase-1A1 (UGT1A1), which metabolizes raltegravir, but the magnitude of steady-state inhibition and role of the UGT1A1 genotype are unknown.	Raltegravir Potassium	79-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-50
20823282-1	2010	Atazanavir inhibits UDP-glucuronyl-transferase-1A1 (UGT1A1), which metabolizes raltegravir, but the magnitude of steady-state inhibition and role of the UGT1A1 genotype are unknown.	Raltegravir Potassium	79-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
20668247-0	2010	Bilirubin glucuronidation revisited: proper assay conditions to estimate enzyme kinetics with recombinant UGT1A1.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
20709051-0	2010	The effect of UGT1A1 promoter polymorphism on bilirubin response to hydroxyurea therapy in hemoglobinopathies.	Bilirubin	46-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
20709051-0	2010	The effect of UGT1A1 promoter polymorphism on bilirubin response to hydroxyurea therapy in hemoglobinopathies.	Hydroxyurea	68-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
20709051-2	2010	However, the effect of hydroxyurea on hyperbilirubinemia in relation to the UGT1A1 gene promoter polymorphism is not known in Indian patients with different hemoglobinopathies.	Hydroxyurea	23-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
20668247-1	2010	Bilirubin, an end product of heme catabolism, is primarily eliminated via glucuronic acid conjugation by UGT1A1.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
20668247-1	2010	Bilirubin, an end product of heme catabolism, is primarily eliminated via glucuronic acid conjugation by UGT1A1.	Glucuronic Acid	74-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
20668247-2	2010	Impaired bilirubin conjugation, caused by inhibition of UGT1A1, can result in clinical consequences, including jaundice and kernicterus.	Bilirubin	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
20668247-3	2010	Thus, evaluation of the ability of new drug candidates to inhibit UGT1A1-catalyzed bilirubin glucuronidation in vitro has become common practice.	Bilirubin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
20668247-10	2010	In conclusion, establishment of appropriate incubation conditions (i.e., very low protein concentrations and short incubation times) is necessary to properly characterize the kinetics of bilirubin glucuronidation in a recombinant UGT1A1 system.	Bilirubin	187-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
21072184-7	2010	Polymorphisms in ABCC2, ABCG2, UGT1A1, UGT1A9, and SLCO1B1 were found to significantly correlate with flavopiridol PK in univariate analysis.	alvocidib	102-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
20890421-11	2010	Our data suggest that atazanavir-associated hyperbilirubinemia is common but transient in a population with low UGT1A1*28 allele frequency.	Atazanavir Sulfate	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
20693308-9	2010	SUMMARY: Serum bilirubin has a protective effect on CVD and CVD-related diseases, and UGT1A1 is the major gene controlling serum bilirubin concentrations.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
20890421-0	2010	Incidence of atazanavir-associated hyperbilirubinemia in Korean HIV patients: 30 months follow-up results in a population with low UDP-glucuronosyltransferase1A1*28 allele frequency.	Atazanavir Sulfate	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-161
20693308-7	2010	A conditional linkage study indicates that UGT1A1 is the major gene controlling serum bilirubin concentrations, and this finding has been confirmed in recent genomewide association studies.	Bilirubin	86-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
20666626-3	2010	Estradiol-3-O-glucuronide (E-3-G) formation was used as the index of UGT1A1 activity.	estradiol-3-o-glucuronide	0-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
20397195-6	2010	UGT1A1, 1A3 and 1A8 had the highest activities and gave rise to the phenolic glucuronide, whereas glucuronidation of the aliphatic hydroxyl group was mostly mediated by UGT2B7 with low activity.	Glucuronides	77-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
20397195-6	2010	UGT1A1, 1A3 and 1A8 had the highest activities and gave rise to the phenolic glucuronide, whereas glucuronidation of the aliphatic hydroxyl group was mostly mediated by UGT2B7 with low activity.	aliphatic hydroxyl	121-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
20890421-2	2010	UDP-glucuronosyltransferase 1A1 polymorphism, UGT1A1*28, which is associated with atazanavir-induced hyperbilirubinemia, is less common in Asians than in Caucasians.	Atazanavir Sulfate	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
20890421-2	2010	UDP-glucuronosyltransferase 1A1 polymorphism, UGT1A1*28, which is associated with atazanavir-induced hyperbilirubinemia, is less common in Asians than in Caucasians.	Atazanavir Sulfate	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
20061399-1	2010	Alterations in the hepatic conjugation of bilirubin due to uridyl-diphosphate-glucuronosyltransferase 1A1 (UGT1A1) polymorphisms have been proposed as risk factors to neonatal jaundice.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-105
20061399-1	2010	Alterations in the hepatic conjugation of bilirubin due to uridyl-diphosphate-glucuronosyltransferase 1A1 (UGT1A1) polymorphisms have been proposed as risk factors to neonatal jaundice.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
20666626-3	2010	Estradiol-3-O-glucuronide (E-3-G) formation was used as the index of UGT1A1 activity.	e-3-g	27-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
20639394-4	2010	In a conditional analysis adjusted for the top UGT1A1 variant (rs11891311), another variant in UGT1A1 (rs4148323, P = 1.22 x 10(-121)) remained significant; this suggests that in UGT1A1 at least two independent genetic variations influence the bilirubin levels in the Korean population.	Bilirubin	244-253	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
20639394-4	2010	In a conditional analysis adjusted for the top UGT1A1 variant (rs11891311), another variant in UGT1A1 (rs4148323, P = 1.22 x 10(-121)) remained significant; this suggests that in UGT1A1 at least two independent genetic variations influence the bilirubin levels in the Korean population.	Bilirubin	244-253	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
20516255-6	2010	The kinetic parameters of BZA-4"-glucuronide formation were determined in liver, duodenum, and jejunum microsomes and with UGT1A1, 1A8, and 1A10, the most active UGT isoforms involved in the glucuronidation of BZA, whereas those of BZA-5-glucuronide were determined with all the enzyme systems except in liver microsomes and in UGT1A1 because the formation of the BZA-5-glucuronide was too low.	bza-4"-glucuronide	26-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
20516255-6	2010	The kinetic parameters of BZA-4"-glucuronide formation were determined in liver, duodenum, and jejunum microsomes and with UGT1A1, 1A8, and 1A10, the most active UGT isoforms involved in the glucuronidation of BZA, whereas those of BZA-5-glucuronide were determined with all the enzyme systems except in liver microsomes and in UGT1A1 because the formation of the BZA-5-glucuronide was too low.	bza-4"-glucuronide	26-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	328-334
20516255-7	2010	K(m) values in liver, duodenum, and jejunum microsomes and UGT1A1, 1A8, and 1A10, were similar and ranged from 5.1 to 33.1 microM for BZA-4"-glucuronide formation and from 2.5 to 11.1 microM for BZA-5-glucuronide formation.	bza-4"-glucuronide	134-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
20643254-0	2010	Relation of ADRB1, CYP2D6, and UGT1A1 polymorphisms with dose of, and response to, carvedilol or metoprolol therapy in patients with chronic heart failure.	Carvedilol	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
21092520-3	2010	The uridine diphosphate-glucuronosyl transferase 1A1 (UGT 1A1) gene controls bilirubin conjugation by determining the structure of the enzyme glucuronosyltransferase, which is synthesized in the hepatocyte.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-52
21092520-3	2010	The uridine diphosphate-glucuronosyl transferase 1A1 (UGT 1A1) gene controls bilirubin conjugation by determining the structure of the enzyme glucuronosyltransferase, which is synthesized in the hepatocyte.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-61
20546738-8	2010	RESULTS: In Gunn rats, bilirubin levels normalized 2 weeks after administration of mTTR.hUGT1A1.	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-95
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	7-hydroxy-4-trifluoromethylcoumarin	86-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	7-hydroxy-4-trifluoromethylcoumarin	123-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	Estradiol	131-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	e-3oh	164-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	Irinotecan	175-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	Irinotecan	207-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-9	2010	In recombinant UGT1A1 enzymes expressed in insect cells, the kinetics of 7-HFC, E-3OH and SN-38 glucuronidation fitted the substrate inhibition (7-HFC glucuronidation) or Hill equation (E-3OH and SN-38 glucuronidation), and each glucuronidation showed the same kinetic profile between humans and cynomolgus monkeys.	3oh	82-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
20620155-9	2010	In recombinant UGT1A1 enzymes expressed in insect cells, the kinetics of 7-HFC, E-3OH and SN-38 glucuronidation fitted the substrate inhibition (7-HFC glucuronidation) or Hill equation (E-3OH and SN-38 glucuronidation), and each glucuronidation showed the same kinetic profile between humans and cynomolgus monkeys.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
20620155-9	2010	In recombinant UGT1A1 enzymes expressed in insect cells, the kinetics of 7-HFC, E-3OH and SN-38 glucuronidation fitted the substrate inhibition (7-HFC glucuronidation) or Hill equation (E-3OH and SN-38 glucuronidation), and each glucuronidation showed the same kinetic profile between humans and cynomolgus monkeys.	Tin	90-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
20643254-0	2010	Relation of ADRB1, CYP2D6, and UGT1A1 polymorphisms with dose of, and response to, carvedilol or metoprolol therapy in patients with chronic heart failure.	Metoprolol	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
20643254-2	2010	The purpose of the present study was to determine whether specific genetic polymorphisms in ADRB1 (encoding the beta1-adrenergic receptor), CYP2D6, and UGT1A1 correlated with dose of, or response to, metoprolol or carvedilol treatment in patients with heart failure.	Metoprolol	200-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
20643254-2	2010	The purpose of the present study was to determine whether specific genetic polymorphisms in ADRB1 (encoding the beta1-adrenergic receptor), CYP2D6, and UGT1A1 correlated with dose of, or response to, metoprolol or carvedilol treatment in patients with heart failure.	Carvedilol	214-224	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
20412608-9	2010	In addition, UGT1A1 expression induced by UCB in Caco-2 cells could ameliorate the cytotoxicity of UCB.	ucb	42-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
20406168-5	2010	In recent years, genetic polymorphisms in UDP-glucuronosyltransferase (UGT) 1A1, an enzyme involved in SN-38 glucuronidation, has been linked to interindividual pharmacokinetic variability and irinotecan toxicity.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-79
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	158-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-89
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	158-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	190-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-89
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	190-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
20562211-0	2010	Dose-dependent association between UGT1A1*28 genotype and irinotecan-induced neutropenia: low doses also increase risk.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
20562211-1	2010	PURPOSE: A previous meta-analysis showed that the association between the UGT1A1*28 genotype and irinotecan-induced neutropenia was influenced by irinotecan dose and that the risk of neutropenia was similar at low doses for patients with all genotypes.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
20562211-1	2010	PURPOSE: A previous meta-analysis showed that the association between the UGT1A1*28 genotype and irinotecan-induced neutropenia was influenced by irinotecan dose and that the risk of neutropenia was similar at low doses for patients with all genotypes.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
20562211-5	2010	The association between UGT1A1*28 and the relative extent of glucuronidation (REG) of SN-38 was also examined.	Irinotecan	86-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
20562211-12	2010	CONCLUSIONS: In conclusion, the UGT1A1*28/*28 genotype was associated with an increased risk of neutropenia not only at medium or high doses of irinotecan but also at low doses.	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
20562211-13	2010	The dose-dependent manner of SN-38 glucuronidation explained why the association between UGT1A1*28 and neutropenia was dose dependent.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
20406168-5	2010	In recent years, genetic polymorphisms in UDP-glucuronosyltransferase (UGT) 1A1, an enzyme involved in SN-38 glucuronidation, has been linked to interindividual pharmacokinetic variability and irinotecan toxicity.	Irinotecan	193-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-79
20063115-10	2010	SN-38 C(max) and AUC in EIAC patients receiving 400 mg/m(2) irinotecan were 20.9 ng/ml and 212 ng/ml h, and in non-EIAC patients receiving 125 mg/m(2), 15.5 ng/ml and 207 ng/ml h. SN-38 AUC varied by UGT1A1*28 status in non-EIAC patients.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	200-206
20562445-2	2010	A major reason for the variability is a common promoter polymorphism, UGT1A1*28, which reduces the transcription of the enzyme that conjugates bilirubin, UDP-glucuronosyltransferase 1A1.	Bilirubin	143-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
20562445-2	2010	A major reason for the variability is a common promoter polymorphism, UGT1A1*28, which reduces the transcription of the enzyme that conjugates bilirubin, UDP-glucuronosyltransferase 1A1.	Bilirubin	143-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-185
20063115-12	2010	Non-EIAC patients with UGT1A1*28 variant alleles appear particularly sensitive to toxicity from irinotecan.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
20580994-0	2010	The UGT1A1*28 polymorphism correlates with erlotinib"s effect on SN-38 glucuronidation.	Erlotinib Hydrochloride	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
20637356-4	2010	The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan.	Fluorouracil	183-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
20637356-4	2010	The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan.	Irinotecan	192-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
20335017-9	2010	The risk of severe diarrhoea at medium and high irinotecan doses was higher among patients with a UGT1A1*28/*28 genotype than among those with a UGT1A1*1/*1 genotype (OR=3.69, 95% confidence interval [CI]=2.00-6.83; P&lt;0.001).	Irinotecan	48-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
20335017-12	2010	In conclusion, patients carrying UGT1A1*28 allele(s) are at an increased risk of irinotecan-induced severe diarrhoea.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
20207085-5	2010	Recent work has linked PNJ to a specific enzyme polymorphism, a variation of the UGT1A1 gene, in the glucoronidation pathway which is essential for bilirubin metabolism and is strongly correlated with ethnic origin.	glucoronidation	101-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
20207085-5	2010	Recent work has linked PNJ to a specific enzyme polymorphism, a variation of the UGT1A1 gene, in the glucoronidation pathway which is essential for bilirubin metabolism and is strongly correlated with ethnic origin.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
20661248-1	2010	BACKGROUND: Accurate description of current practice within advanced colorectal cancer (CRC) specialties were needed to inform an economic evaluation of the UGT1A1 pharmacogenetic test for irinotecan in the United Kingdom.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
20504240-1	2010	BACKGROUND: High prevalence of severe atazanavir-associated hyperbilirubinemia in Asians with low prevalence of the UDP-glucuronosyltransferase (UGT)1A1*28 polymorphism suggests the importance of genetic factors other than UGT1A1*28 for atazanavir-associated hyperbilirubinemia in these populations.	Atazanavir Sulfate	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	223-229
20504240-1	2010	BACKGROUND: High prevalence of severe atazanavir-associated hyperbilirubinemia in Asians with low prevalence of the UDP-glucuronosyltransferase (UGT)1A1*28 polymorphism suggests the importance of genetic factors other than UGT1A1*28 for atazanavir-associated hyperbilirubinemia in these populations.	Atazanavir Sulfate	237-247	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-152
20504240-10	2010	CONCLUSION: The MDR1 G2677T/A variation and UGT1A1*28 are independent risk factors for severe atazanavir-associated hyperbilirubinemia in Korean human immunodeficiency virus-infected patients.	Atazanavir Sulfate	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
20335017-0	2010	Dose-dependent association between UGT1A1*28 polymorphism and irinotecan-induced diarrhoea: a meta-analysis.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
20335017-2	2010	The associations between the UGT1A1*28 polymorphism and irinotecan-induced diarrhoea remains controversial because of conflicting data in the literature.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
20580994-0	2010	The UGT1A1*28 polymorphism correlates with erlotinib"s effect on SN-38 glucuronidation.	Irinotecan	65-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
20580994-6	2010	Our data showed that erlotinib exhibited potent non-competitive inhibition against SN-38 glucuronidation in pooled HLMs and UGT1A1.	Erlotinib Hydrochloride	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
20580994-6	2010	Our data showed that erlotinib exhibited potent non-competitive inhibition against SN-38 glucuronidation in pooled HLMs and UGT1A1.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
20580994-7	2010	Using the physiological and pharmacokinetic parameters obtained from the literature, we estimated the in vivo concentrations of unbound erlotinib available for UGT1A1 active site and thus the AUC ratios of SN-38 were also quantitatively predicted.	Erlotinib Hydrochloride	136-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
20580994-9	2010	Significant correlations were observed between SN-38 glucuronidation activity in the presence of erlotinib and UGT1A1*28 in 52 Caucasian liver microsomes.	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
20580994-10	2010	Our results suggest that erlotinib is a potent inhibitor of SN-38 glucuronidation via UGT1A1 inhibition.	Erlotinib Hydrochloride	25-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
20580994-10	2010	Our results suggest that erlotinib is a potent inhibitor of SN-38 glucuronidation via UGT1A1 inhibition.	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
20580994-12	2010	UGT1A1*28 polymorphism correlates with erlotinib"s effect on SN-38 glucuronidation.	Erlotinib Hydrochloride	39-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
20580994-12	2010	UGT1A1*28 polymorphism correlates with erlotinib"s effect on SN-38 glucuronidation.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
20435641-3	2010	To elucidate these molecular mechanisms, we simulated and analysed the glucuronidation of wild-type UGT1A1 and six UGT1A1 mutants, with bilirubin as the substrate.	Bilirubin	136-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
20308029-2	2010	Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is a main metabolic pathway of estrogen detoxification in steroid target tissues, such as the prostate.	Steroids	140-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-64
20979879-3	2010	The phenobarbital-responsive enhancer module (PBREM), TATA box and common mutation sites in exons of UGT1A1 gene were amplified by polymerase chain reaction (PCR) and the products screened by direct DNA sequencing.	Phenobarbital	4-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
20297805-4	2010	The results also indicated that UGT1A1, UGT1A7, UGT1A8, UGT1A9, UGT1A10 and UGT2B7 are the most important six UGT isoforms for metabolizing the chosen flavones.	Flavones	151-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
20602618-3	2010	Although multiple genes may play a role in irinotecan activity, the majority of evidence to date suggests that variation in expression of UGT1A1 caused by a common promoter polymorphism (UGT1A1*28) is strongly associated with toxicity; however, this link is dose dependent.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
20602618-3	2010	Although multiple genes may play a role in irinotecan activity, the majority of evidence to date suggests that variation in expression of UGT1A1 caused by a common promoter polymorphism (UGT1A1*28) is strongly associated with toxicity; however, this link is dose dependent.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
20370320-2	2010	Several clinical and epidemiological studies have been carried out on key enzymes generating and eliminating bilirubin (heme oxygenase-1 and UDP-glucuronosyltransferase UGT1A1, respectively) and their regulation by the AhR.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
20308029-2	2010	Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is a main metabolic pathway of estrogen detoxification in steroid target tissues, such as the prostate.	Steroids	140-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
20215562-4	2010	Here, we present a homology model of the complete monomeric human UGT1A1, the enzyme that catalyzes bilirubin glucuronidation.	Bilirubin	100-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
20022574-2	2010	In particular, polymorphisms across three genes involved in bilirubin production and metabolism [glucose-6-phosphate dehydrogenase (G6PD), uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and solute carrier organic anion transporter polypeptide 1B1 (SLCO1B1)] may interact with each other and/or environmental contributors to produce significant hyperbilirubinemia.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-187
20022574-2	2010	In particular, polymorphisms across three genes involved in bilirubin production and metabolism [glucose-6-phosphate dehydrogenase (G6PD), uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and solute carrier organic anion transporter polypeptide 1B1 (SLCO1B1)] may interact with each other and/or environmental contributors to produce significant hyperbilirubinemia.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
20207827-0	2010	Pegvisomant-induced liver injury is related to the UGT1A1*28 polymorphism of Gilbert"s syndrome.	pegvisomant	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
19771428-2	2010	METHODS: Associations between transporter haplotypes/variations along with UGT1A1*28 or *6 and SN-38 area under the time-concentration curve (AUC) or neutropenia were examined in irinotecan monotherapy (55 patients) and irinotecan-cisplatin-combination therapy (62 patients).	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
20207827-12	2010	CONCLUSIONS: The UGT1A1*28 genotype and male gender predict an increased incidence of LFT abnormalities during PEG therapy in acromegaly.	pegvisomant	111-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
20056724-4	2010	UGT1A9, UGT1A1, UGT1A7, UGT1A8, and UGT1A3 are the major enzymes catalyzing hesperetin glucuronidation, the latter only producing 7-O-glucuronide, whereas UGT1A7 produced mainly 3"-O-glucuronide.	hesperetin	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
20513938-3	2010	Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
20513938-3	2010	Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively.	Fluorouracil	95-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
20513938-3	2010	Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively.	Fluorouracil	111-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
20389299-0	2010	Pazopanib-induced hyperbilirubinemia is associated with Gilbert"s syndrome UGT1A1 polymorphism.	pazopanib	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
20389299-7	2010	The Gilbert"s uridine-diphosphoglucuronate glucuronosyltransferase 1A1 (UGT1A1) TA-repeat polymorphism was significantly associated with pazopanib-induced hyperbilirubinemia in the phase II study.	pazopanib	137-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-70
20389299-7	2010	The Gilbert"s uridine-diphosphoglucuronate glucuronosyltransferase 1A1 (UGT1A1) TA-repeat polymorphism was significantly associated with pazopanib-induced hyperbilirubinemia in the phase II study.	pazopanib	137-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
20389299-12	2010	CONCLUSIONS: The UGT1A1 polymorphism is frequently associated with pazopanib-induced hyperbilirubinemia.	pazopanib	67-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
20056724-4	2010	UGT1A9, UGT1A1, UGT1A7, UGT1A8, and UGT1A3 are the major enzymes catalyzing hesperetin glucuronidation, the latter only producing 7-O-glucuronide, whereas UGT1A7 produced mainly 3"-O-glucuronide.	7-o-glucuronide	130-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
20056724-4	2010	UGT1A9, UGT1A1, UGT1A7, UGT1A8, and UGT1A3 are the major enzymes catalyzing hesperetin glucuronidation, the latter only producing 7-O-glucuronide, whereas UGT1A7 produced mainly 3"-O-glucuronide.	3"-o-glucuronide	178-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
20511137-3	2010	Numerous variants have been found in UGT1A1 , the main conjugating enzyme of bilirubin and drugs such as the anticancer drug irinotecan.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
20511137-3	2010	Numerous variants have been found in UGT1A1 , the main conjugating enzyme of bilirubin and drugs such as the anticancer drug irinotecan.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
20511137-4	2010	Recently, the US Food and Drug Administration (FDA) recommended testing for the presence of UGT1A1*28 , an allele correlated with decreased transcriptional activity, to predict patients at risk of irinotecan toxicity.	Irinotecan	197-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
20197307-2	2010	The constitutive androstane receptor (CAR) is an orphan nuclear receptor that has been shown to participate in the activation of the uridine diphosphate-5"-glucuronosyltransferase 1A1 (UGT1A1) gene, which plays an important role in bilirubin clearance.	Bilirubin	232-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-183
20179984-0	2010	Indispensability of UGT1A1*6 genotyping in Japanese cancer patients treated with irinotecan.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
20197307-2	2010	The constitutive androstane receptor (CAR) is an orphan nuclear receptor that has been shown to participate in the activation of the uridine diphosphate-5"-glucuronosyltransferase 1A1 (UGT1A1) gene, which plays an important role in bilirubin clearance.	Bilirubin	232-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
20197307-7	2010	These data suggest that OSM might play a role in bilirubin metabolism via the CAR-UGT1A1 pathway.	Bilirubin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
19932091-1	2010	BACKGROUND: The basis of Gilbert"s syndrome is a 70% reduction in bilirubin glucuronidation which, in the Caucasian population, is the result of a homozygous TA insertion into the promoter region of the UDP-glucuronosyltransferase 1A1 (UGT1A1) gene (UGT1A128 allele).	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
20057336-1	2010	The uridine diphosphoglucuronate-glucuronosyltransferase 1A1 (UGT1A1) gene encodes the enzyme responsible for bilirubin glucuronidation.	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-60
20057336-1	2010	The uridine diphosphoglucuronate-glucuronosyltransferase 1A1 (UGT1A1) gene encodes the enzyme responsible for bilirubin glucuronidation.	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
20194756-1	2010	High levels of unconjugated bilirubin (UCB) in newborn children is associated with a reduction in hepatic UDP glucuronosyltransferase (UGT) 1A1 activity that can lead to CNS toxicity, brain damage, and even death.	Bilirubin	28-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-143
20194756-1	2010	High levels of unconjugated bilirubin (UCB) in newborn children is associated with a reduction in hepatic UDP glucuronosyltransferase (UGT) 1A1 activity that can lead to CNS toxicity, brain damage, and even death.	ucb	39-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-143
20145913-4	2010	The assays are based on analysis and quantification by high-performance liquid chromatography-tandem mass spectrometry of glucuronides formed from selective probe substrates, namely, beta-estradiol (UGT1A1, 3-glucuronide), 1-naphthol (UGT1A6), propofol (UGT1A9), and naloxone (UGT2B7).	Glucuronides	122-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
20145913-4	2010	The assays are based on analysis and quantification by high-performance liquid chromatography-tandem mass spectrometry of glucuronides formed from selective probe substrates, namely, beta-estradiol (UGT1A1, 3-glucuronide), 1-naphthol (UGT1A6), propofol (UGT1A9), and naloxone (UGT2B7).	Estradiol	183-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
20235794-2	2010	Irinotecan is one of the models for personalized medicine based on pharmacogenetics, and a number of clinical studies have revealed significant associations between UGT1A1*28 and irinotecan toxicity.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
20235794-2	2010	Irinotecan is one of the models for personalized medicine based on pharmacogenetics, and a number of clinical studies have revealed significant associations between UGT1A1*28 and irinotecan toxicity.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
20038727-1	2010	PURPOSE We aimed to identify the maximum-tolerated dose (MTD) of irinotecan in patients with cancer with UGT1A1*1/*1 and *1/*28 genotypes.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
19996319-2	2010	Initially, using an inducible system that mimics the relative abundance of isoforms 1 and 2 of UGT1A1 in human tissues, the rates of formation of glucuronides were significantly reduced.	Glucuronides	146-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
19953640-3	2010	Crigler-Najjar syndrome is another rare disorder of bilirubin metabolism caused by mutation in the gene coding the enzyme UGT1A1.	Bilirubin	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
19931474-0	2010	Hereditary spherocytosis and the (TA)nTAA polymorphism of UGT1A1 gene promoter region--a comparison of the bilirubin plasmatic levels in the different clinical forms.	Bilirubin	107-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
20028383-1	2010	Although individuals carrying the UGT1A1 allele *28 have an increased risk of severe toxicities associated with irinotecan, no phase I study has been conducted based on the polymorphism.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
20028383-12	2010	The recommended starting doses of biweekly irinotecan for phase II/III were 150 mg/m(2) for patients with the UGT1A1 6/6 genotype and 70 mg/m(2) for those with the 6/7 genotype, respectively.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
20235794-5	2010	This article provides an overview of recent progress in irinotecan pharmacogenetics and discusses the clinical significance of the UGT1A1 genotype/haplotype with regard to severe irinotecan toxicity.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
19932091-1	2010	BACKGROUND: The basis of Gilbert"s syndrome is a 70% reduction in bilirubin glucuronidation which, in the Caucasian population, is the result of a homozygous TA insertion into the promoter region of the UDP-glucuronosyltransferase 1A1 (UGT1A1) gene (UGT1A128 allele).	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	236-242
19744523-8	2010	Other well-established associations include CYP2B6 alleles and efavirenz central nervous system side effects, UGT1A1 alleles and atazanavir-associated hyperbilirubinemia and HLA class II allele HLA-DRB*0101 and nevirapine-associated hypersensitivity.	Atazanavir Sulfate	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-43
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-43
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
20096102-3	2010	Interestingly, one of these CpG dinucleotides (CpG -4) is found close to a HNF1 response element (HRE), known to be involved in activation of UGT1A1 gene expression, and within an upstream stimulating factor (USF) binding site.	Dinucleoside Phosphates	32-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
20000589-3	2010	Screening of indole metabolites has identified indoxyl 3-sulfate (I3S) as a potent endogenous ligand that selectively activates the human AHR at nanomolar concentrations in primary human hepatocytes, regulating transcription of multiple genes, including CYP1A1, CYP1A2, CYP1B1, UGT1A1, UGT1A6, IL6, and SAA1.	indoxyl 3-sulfate	47-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	278-284
20000589-3	2010	Screening of indole metabolites has identified indoxyl 3-sulfate (I3S) as a potent endogenous ligand that selectively activates the human AHR at nanomolar concentrations in primary human hepatocytes, regulating transcription of multiple genes, including CYP1A1, CYP1A2, CYP1B1, UGT1A1, UGT1A6, IL6, and SAA1.	inositol 1,3,4-trisphosphate	66-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	278-284
20371435-0	2010	Coexistence of HFE and rare UGT1A1 genes mutations in patients with iron overload related liver injury.	Iron	68-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
19788348-9	2010	7-OHWAR was a high-affinity substrate for UGT1A1, compared to other UGTs.	7-ohwar	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
19788348-10	2010	UGT1A1 and UGT1A10 also glucuronidated 6-OHWAR.	6-ohwar	39-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19955297-8	2010	DISCUSSION: Atazanavir is an inhibitor of the bilirubin-conjugating enzyme UGT1A1 and has been frequently linked to the occurrence of hyperbilirubinemia without complications.	Atazanavir Sulfate	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
19955297-8	2010	DISCUSSION: Atazanavir is an inhibitor of the bilirubin-conjugating enzyme UGT1A1 and has been frequently linked to the occurrence of hyperbilirubinemia without complications.	Bilirubin	46-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
19850672-5	2010	Erlotinib exhibited selective potent competitive inhibition against 4-MU glucuronidation by UGT1A1, and gefitinib demonstrated a wide range of inhibition against UGT-mediated 4-MU glucuronidation, particularly against UGT1A1, UGT1A7, UGT1A9, and UGT2B7.	Erlotinib Hydrochloride	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19796502-2	2010	Among these, urea cycle disorders leading to the impairment to detoxify ammonia and Crigler-Najjar Syndrome type I, a deficiency in the hepatic UDP-glucuronosyltransferase 1A1 present the highest incidence.	Ammonia	72-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-175
19796502-6	2010	Moreover, the evaluation of urea synthesis from ammonia and UDP-glucuronosyltransferase 1A1 activity, a newly developed assay using beta-estradiol as substrate, allows the possibility of customizing cell preparation for receptors with urea cycle disorders or Crigler-Najjar Syndrome type I.	Estradiol	132-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-91
20948202-2	2010	A major cause of elevated plasma bilirubin is the common UGT1A1*28 promoter polymorphism in the gene of the bilirubin-conjugating enzyme UDP-glucuronosyltransferase 1A1, which reduces transcription by 70%.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
20948202-2	2010	A major cause of elevated plasma bilirubin is the common UGT1A1*28 promoter polymorphism in the gene of the bilirubin-conjugating enzyme UDP-glucuronosyltransferase 1A1, which reduces transcription by 70%.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-168
20948202-2	2010	A major cause of elevated plasma bilirubin is the common UGT1A1*28 promoter polymorphism in the gene of the bilirubin-conjugating enzyme UDP-glucuronosyltransferase 1A1, which reduces transcription by 70%.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
20948202-2	2010	A major cause of elevated plasma bilirubin is the common UGT1A1*28 promoter polymorphism in the gene of the bilirubin-conjugating enzyme UDP-glucuronosyltransferase 1A1, which reduces transcription by 70%.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-168
20948202-8	2010	The UGT1A1*28 polymorphism (allele frequency 30%) showed a strong gene-dose relationship with bilirubin levels both among cases and referents, but was not associated with risk for stroke.	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19794410-5	2010	Surprisingly, lactone formation was significantly higher in carriers of UGT1A1*28, an allele that is associated with lower UGT1A1 expression.	Lactones	14-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
19794410-5	2010	Surprisingly, lactone formation was significantly higher in carriers of UGT1A1*28, an allele that is associated with lower UGT1A1 expression.	Lactones	14-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
19797611-2	2010	Treatment with 1,4-diamino-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126) (an extracellular signal-regulated kinase inhibitor) suppressed the HGF-induced expression of UGT1A1 and CYP2B6, as well as p16, p21, and p27 in HepG2 cells.	u0124	15-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
19797611-2	2010	Treatment with 1,4-diamino-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126) (an extracellular signal-regulated kinase inhibitor) suppressed the HGF-induced expression of UGT1A1 and CYP2B6, as well as p16, p21, and p27 in HepG2 cells.	U 0126	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
19797611-3	2010	The CDK inhibitor roscovitine also enhanced the expression of UGT1A1, CYP2B6, and CYP3A4.	Roscovitine	18-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
19835560-6	2010	Variant alleles of UGT1A1 are less capable of conjugating and eliminating SN-38, the active form of the topoisomerase inhibitor irinotecan, and defective alleles for NAT2 are responsible for the well-described acetylation polymorphism that leads to impaired clearance of isoniazid and other agents.	Irinotecan	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
19835560-6	2010	Variant alleles of UGT1A1 are less capable of conjugating and eliminating SN-38, the active form of the topoisomerase inhibitor irinotecan, and defective alleles for NAT2 are responsible for the well-described acetylation polymorphism that leads to impaired clearance of isoniazid and other agents.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
19835560-6	2010	Variant alleles of UGT1A1 are less capable of conjugating and eliminating SN-38, the active form of the topoisomerase inhibitor irinotecan, and defective alleles for NAT2 are responsible for the well-described acetylation polymorphism that leads to impaired clearance of isoniazid and other agents.	Isoniazid	271-280	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
19797611-6	2010	In cells arrested in S phase by a thymidine block and then released into a synchronous cell cycle, there was a clear dissociation among the activation of CDK2 and the expression of UGT1A1, CYP2B6, and CYP3A4.	Thymidine	34-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-187
19850672-5	2010	Erlotinib exhibited selective potent competitive inhibition against 4-MU glucuronidation by UGT1A1, and gefitinib demonstrated a wide range of inhibition against UGT-mediated 4-MU glucuronidation, particularly against UGT1A1, UGT1A7, UGT1A9, and UGT2B7.	Erlotinib Hydrochloride	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	218-224
19850672-5	2010	Erlotinib exhibited selective potent competitive inhibition against 4-MU glucuronidation by UGT1A1, and gefitinib demonstrated a wide range of inhibition against UGT-mediated 4-MU glucuronidation, particularly against UGT1A1, UGT1A7, UGT1A9, and UGT2B7.	Gefitinib	104-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	218-224
19850672-7	2010	We estimated that coadministration of erlotinib at 100 mg/day or higher doses may result in at least a 30% increase in the AUC of drugs predominantly cleared by UGT1A1.	Erlotinib Hydrochloride	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
19850672-8	2010	Thus, the coadministration of erlotinib with drugs primarily cleared by UGT1A1 may result in potential DDI.	Erlotinib Hydrochloride	30-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
20201778-3	2010	The system was then validated using known ligands of PXR, rifampicin (RIF), clotrimazole (CLOT) sulfinpyrazone (SPZ) and phenobarbital (PB), which produced dose dependent induction of UGT1A1 luciferase activity by 4.4, 5.3, 4.7 and 3.7 fold, respectively, relative to the vehicle control, 0.1 % dimethylsulfoxide (DMSO).	clotrimazole (clot) sulfinpyrazone	76-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	184-190
19830808-7	2010	In addition to bilirubin, we also determined their activity toward eight other UGT1A1 substrates.	Bilirubin	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
20201778-3	2010	The system was then validated using known ligands of PXR, rifampicin (RIF), clotrimazole (CLOT) sulfinpyrazone (SPZ) and phenobarbital (PB), which produced dose dependent induction of UGT1A1 luciferase activity by 4.4, 5.3, 4.7 and 3.7 fold, respectively, relative to the vehicle control, 0.1 % dimethylsulfoxide (DMSO).	Phenobarbital	121-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	184-190
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	a-naphthoflavone	40-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	a-naphthoflavone	40-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	a-naph	58-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	a-naph	58-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	beta-Naphthoflavone	67-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	beta-Naphthoflavone	67-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	b-naph	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	b-naph	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	3-methylchloranthene	97-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	3-methylchloranthene	97-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
20722998-0	2010	Glucuronidation of piceatannol by human liver microsomes: major role of UGT1A1, UGT1A8 and UGT1A10.	3,3',4,5'-tetrahydroxystilbene	19-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
19475557-9	2010	Coexpression of UGT2B7 also affected the kinetics of estradiol 3-O-glucuronidation by UGT1A1, imipramine N-glucuronidation by UGT1A4, serotonin O-glucuronidation by UGT1A6, and propofol O-glucuronidation by UGT1A9.	estradiol 3-o	53-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
20402064-4	2010	Thymine-adenine (TA) repeats in the promoter region of the UGT1A1 gene were investigated by polymerase chain reaction (PCR)-based non-radioactive DNA sequencing.	thymine-adenine	0-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
21486535-1	2010	PURPOSE: Functional polymorphisms of the UGT1A1 gene, particularly the UGT1A1*28 variant, are associated with the severity of the bone marrow suppression in patients with metastatic colorectal cancer receiving irinotecan.	Irinotecan	210-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
21486535-1	2010	PURPOSE: Functional polymorphisms of the UGT1A1 gene, particularly the UGT1A1*28 variant, are associated with the severity of the bone marrow suppression in patients with metastatic colorectal cancer receiving irinotecan.	Irinotecan	210-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
20358470-4	2010	We also explored the association between the UGT1A1*28 polymorphism and serum bilirubin concentrations and DNA damage and repair measures.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
20377135-0	2010	The UGT1A1*28 genotype and the toxicity of low-dose irinotecan in patients with advanced lung cancer.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
20377135-1	2010	The association between the UGT1A1*28 genotype and the severe toxicity of low-dose irinotecan has been controversial, and few studies have examined this association in patients with lung cancer.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20377135-2	2010	The aim of this study was to assess the association between the UGT1A1*28 genotype and the severe toxicity of low-dose irinotecan in Japanese patients with lung cancer.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
20377135-11	2010	Therefore, low-dose irinotecan could be administered without reducing starting dose in patients with UGT1A1*28 genotype.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
20402064-4	2010	Thymine-adenine (TA) repeats in the promoter region of the UGT1A1 gene were investigated by polymerase chain reaction (PCR)-based non-radioactive DNA sequencing.	Tantalum	17-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
19608554-0	2009	Prolonged neutropenia after irinotecan-based chemotherapy in a child with polymorphisms of UGT1A1 and SLCO1B1.	Irinotecan	28-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
19608554-1	2009	Genetic polymorphisms of uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and SLCO1B1 coding organic anion-transporter polypeptide 1B1, are independent risk factors known to increase irinotecan toxicity in adults.	Irinotecan	193-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-73
19608554-1	2009	Genetic polymorphisms of uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and SLCO1B1 coding organic anion-transporter polypeptide 1B1, are independent risk factors known to increase irinotecan toxicity in adults.	Irinotecan	193-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
19608554-5	2009	To our knowledge, this is the first case report of combined genotyping of both UGT1A1 and SLCO1B1 in a child with severe irinotecan toxicity.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
20071295-2	2009	Its active metabolite, 7-ethyl-10 hydroxycamptothecin (SN-38) is glucuronidated by a uridine-diphosphoglucuronosyltransferase (UGT1A1) to form an inactive metabolite.	Irinotecan	23-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
19415281-8	2009	UGT1A1 polymorphisms were associated with variability in irinotecan PK.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19747074-6	2009	Homeostatic feedback loops might not only include CYP1A1 but also Phase II enzymes such as UGT1A1 which controls the antioxidant AhR ligand bilirubin.	Bilirubin	140-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
19672597-0	2009	UGT1A1 polymorphism and hyperbilirubinemia in a patient who received sorafenib.	Sorafenib	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19672597-1	2009	PURPOSE: To report a single case of uridine glucuronosyltransferase 1A1 (UGT1A1) polymorphism and hyperbilirubinemia in a patient who received sorafenib.	Sorafenib	143-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-71
19672597-1	2009	PURPOSE: To report a single case of uridine glucuronosyltransferase 1A1 (UGT1A1) polymorphism and hyperbilirubinemia in a patient who received sorafenib.	Sorafenib	143-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19672597-8	2009	CONCLUSIONS: The isolated increase in serum bilirubin levels in our patient was probably due to sorafenib-induced UGT1A1 inhibition that manifested itself due both to the patient having one UGT1A1*28 allele and the presence of underlying liver disease.	Bilirubin	44-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
19672597-8	2009	CONCLUSIONS: The isolated increase in serum bilirubin levels in our patient was probably due to sorafenib-induced UGT1A1 inhibition that manifested itself due both to the patient having one UGT1A1*28 allele and the presence of underlying liver disease.	Bilirubin	44-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
19672597-8	2009	CONCLUSIONS: The isolated increase in serum bilirubin levels in our patient was probably due to sorafenib-induced UGT1A1 inhibition that manifested itself due both to the patient having one UGT1A1*28 allele and the presence of underlying liver disease.	Sorafenib	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
19672597-8	2009	CONCLUSIONS: The isolated increase in serum bilirubin levels in our patient was probably due to sorafenib-induced UGT1A1 inhibition that manifested itself due both to the patient having one UGT1A1*28 allele and the presence of underlying liver disease.	Sorafenib	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
19861894-8	2009	Formalin-fixed paraffin-embedded (FFPE) tissue was tested for UGT1A1 promoter variants by polymerase chain reaction and capillary electrophoresis.	Formaldehyde	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
19861894-9	2009	To our knowledge, this is the first study to successfully apply UGT1A1 promoter genotyping to formalin-fixed paraffin-embedded tissue, which may facilitate more thorough examination of clinicopathologic correlations.	Formaldehyde	94-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
19861894-9	2009	To our knowledge, this is the first study to successfully apply UGT1A1 promoter genotyping to formalin-fixed paraffin-embedded tissue, which may facilitate more thorough examination of clinicopathologic correlations.	Paraffin	109-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
20071295-2	2009	Its active metabolite, 7-ethyl-10 hydroxycamptothecin (SN-38) is glucuronidated by a uridine-diphosphoglucuronosyltransferase (UGT1A1) to form an inactive metabolite.	Irinotecan	55-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
20071295-3	2009	It was supposed that patients with the UGT1A1*28 polymorphism would have a greater prevalence of elevated pretreatment serum bilirubin levels and higher toxicity.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
19710077-11	2009	Indirect bilirubin increased 1.6- to 2.8-fold more in subjects with UGT1A1 *28/*28 versus *1/*28 or *1/*1.	Bilirubin	9-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
19732760-0	2009	Haplotypes in the UGT1A1 gene and their role as genetic determinants of bilirubin concentration in healthy German volunteers.	Bilirubin	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
19732760-1	2009	BACKGROUND: Genetic variations of UDP-glucuronyltransferase 1A1 (UGT1A1) influence the concentration of serum bilirubin.	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-63
19732760-1	2009	BACKGROUND: Genetic variations of UDP-glucuronyltransferase 1A1 (UGT1A1) influence the concentration of serum bilirubin.	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
19732760-2	2009	We investigated the association of four common polymorphisms including UGT1A1-53(TA)(n), and common haplotypes of the UGT1A1 gene with bilirubin levels in 218 Caucasian volunteers.	Bilirubin	135-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
19732760-9	2009	Male sex, UGT1A1-53(TA)(6/7) and the c.-3279GG variant were significantly associated with higher bilirubin concentrations.	Bilirubin	97-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
19732760-10	2009	CONCLUSIONS: Two UGT1A1 promoter polymorphisms (-53(TA)(6/7) and c.-3279T&gt;G) and a common haplotype of the UGT1A1 gene are associated with serum bilirubin concentrations in Caucasians.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
19732760-10	2009	CONCLUSIONS: Two UGT1A1 promoter polymorphisms (-53(TA)(6/7) and c.-3279T&gt;G) and a common haplotype of the UGT1A1 gene are associated with serum bilirubin concentrations in Caucasians.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
19948621-2	2009	Variants in the UGT1A1 gene contribute to increased bilirubin levels, and bilirubin can act as an antioxidant.	Bilirubin	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
19948621-2	2009	Variants in the UGT1A1 gene contribute to increased bilirubin levels, and bilirubin can act as an antioxidant.	Bilirubin	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
19770637-0	2009	UGT1A1 genotyping: a predictor of irinotecan-associated side effects and drug efficacy?	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19770637-3	2009	SN-38 is inactivated by uridine disphosphate glucuronosyl transferase 1 (UGT1A1) into the inactive compound SN-38G, which is excreted with the bile.This review concentrates on a critical evaluation of UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19770637-3	2009	SN-38 is inactivated by uridine disphosphate glucuronosyl transferase 1 (UGT1A1) into the inactive compound SN-38G, which is excreted with the bile.This review concentrates on a critical evaluation of UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
19770637-3	2009	SN-38 is inactivated by uridine disphosphate glucuronosyl transferase 1 (UGT1A1) into the inactive compound SN-38G, which is excreted with the bile.This review concentrates on a critical evaluation of UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer.	Irinotecan	301-311	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19811694-6	2009	Resveratrol ranging from 1 to 5 microm could significantly suppress the expressions of cytochrome P450 (CYP) 1A1, CYP1B1 and UDP-glucuronosyltransferase (UGT) 1A1 induced by 7,12-dimethylbenz[a]anthracene (DMBA).	Resveratrol	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-162
19811694-6	2009	Resveratrol ranging from 1 to 5 microm could significantly suppress the expressions of cytochrome P450 (CYP) 1A1, CYP1B1 and UDP-glucuronosyltransferase (UGT) 1A1 induced by 7,12-dimethylbenz[a]anthracene (DMBA).	7,12-dimethylbenz[a	174-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-162
19811694-6	2009	Resveratrol ranging from 1 to 5 microm could significantly suppress the expressions of cytochrome P450 (CYP) 1A1, CYP1B1 and UDP-glucuronosyltransferase (UGT) 1A1 induced by 7,12-dimethylbenz[a]anthracene (DMBA).	anthracene	194-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-162
19710077-15	2009	The wild-type ABCB1 CGC haplotype was associated with slower CL/F and the UGT1A1 *28 genotype was associated with increased bilirubin.	Bilirubin	124-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
19710077-16	2009	Thus, CYP3A5, ABCB1 and UGT1A1 polymorphisms are associated with atazanavir pharmacokinetics and pharmacodynamics in vivo.	Atazanavir Sulfate	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
19732436-9	2009	siRNA treatment against UGT1A also showed an increase in MTX sensitivity.	Methotrexate	57-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-29
19859999-0	2009	UGT1A1 gene polymorphism: impact on toxicity and efficacy of irinotecan-based regimens in metastatic colorectal cancer.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19859999-1	2009	AIM: To investigate the correlation between uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) gene polymorphisms and irinotecan-associated side effects and parameters of drug efficacy in patients with metastatic colorectal cancer (mCRC) receiving a low-dose weekly irinotecan chemotherapeutic regimen.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-92
19859999-1	2009	AIM: To investigate the correlation between uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) gene polymorphisms and irinotecan-associated side effects and parameters of drug efficacy in patients with metastatic colorectal cancer (mCRC) receiving a low-dose weekly irinotecan chemotherapeutic regimen.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
19859999-2	2009	METHODS: Genotypes were retrospectively evaluated by gene scan analysis on the ABI 310 sequencer of the TATAA box in the promoter region of the UGT1A1 gene in blood samples from 105 patients who had received 1st line irinotecan-based chemotherapy for mCRC.	Irinotecan	217-227	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
19859999-7	2009	CONCLUSION: This analysis demonstrates the non-significant influence of the UGT1A1 gene polymorphism on efficacy and rate of irinotecan-associated toxicity in mCRC patients receiving low-dose irinotecan based chemotherapy.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
19389676-0	2009	Conditional linkage and genome-wide association studies identify UGT1A1 as a major gene for anti-atherogenic serum bilirubin levels--the Framingham Heart Study.	Bilirubin	115-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
19389676-10	2009	CONCLUSIONS: Our studies suggest that UGT1A1 may be the major gene with strong effects on bilirubin levels and the TA-repeat polymorphism might be the key polymorphism within the gene controlling bilirubin levels.	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
19389676-10	2009	CONCLUSIONS: Our studies suggest that UGT1A1 may be the major gene with strong effects on bilirubin levels and the TA-repeat polymorphism might be the key polymorphism within the gene controlling bilirubin levels.	Bilirubin	196-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
19487247-0	2009	Influence of N-terminal domain histidine and proline residues on the substrate selectivities of human UDP-glucuronosyltransferase 1A1, 1A6, 1A9, 2B7, and 2B10.	Histidine	31-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-133
19517472-1	2009	BACKGROUND: The objective of this study was to examine the cost effectiveness of using a pharmacogenetic test for uridine diphosphate glycosyltransferase 1A1*28 (UGT1A1*28) variant homozygosity before administering irinotecan to patients with metastatic colorectal cancer.	Irinotecan	215-225	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
19517472-4	2009	With genetic testing, irinotecan dosage was reduced 25% in homozygotes with the UGT1A1*28 variant allele.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
19487247-0	2009	Influence of N-terminal domain histidine and proline residues on the substrate selectivities of human UDP-glucuronosyltransferase 1A1, 1A6, 1A9, 2B7, and 2B10.	Proline	45-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-133
19487247-5	2009	The conserved N-terminal domain histidine of UGT1A1, UGT1A6, UGT1A9, and UGT2B7 was mutated to proline and leucine 34 of UGT2B10 was substituted with histidine, and the capacity of the wild-type and mutant proteins to glucuronidate 4MU, 1NP, LTG, TFP, and naproxen was characterized.	Naproxen	256-264	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19487247-1	2009	An N-terminal domain histidine [corresponding to position 39 of UDP-glucuronosyltransferase (UGT) 1A1] is conserved in all UGT1A and UGT2B subfamily proteins except UGT1A4 (Pro-40) and UGT2B10 (Leu-34).	Histidine	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-101
19487247-6	2009	Whereas UGT1A1(H39P), UGT1A6(H38P), and UGT1A9(H37P) lacked the ability to metabolize 4MU, 1NP, and naproxen, all glucuronidated LTG.	Hymecromone	86-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
19487247-6	2009	Whereas UGT1A1(H39P), UGT1A6(H38P), and UGT1A9(H37P) lacked the ability to metabolize 4MU, 1NP, and naproxen, all glucuronidated LTG.	1-naphthol	91-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
19487247-6	2009	Whereas UGT1A1(H39P), UGT1A6(H38P), and UGT1A9(H37P) lacked the ability to metabolize 4MU, 1NP, and naproxen, all glucuronidated LTG.	Naproxen	100-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-171
19487247-6	2009	Whereas UGT1A1(H39P), UGT1A6(H38P), and UGT1A9(H37P) lacked the ability to metabolize 4MU, 1NP, and naproxen, all glucuronidated LTG.	Lamotrigine	129-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
19487247-1	2009	An N-terminal domain histidine [corresponding to position 39 of UDP-glucuronosyltransferase (UGT) 1A1] is conserved in all UGT1A and UGT2B subfamily proteins except UGT1A4 (Pro-40) and UGT2B10 (Leu-34).	Leucine	194-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-101
19487247-5	2009	The conserved N-terminal domain histidine of UGT1A1, UGT1A6, UGT1A9, and UGT2B7 was mutated to proline and leucine 34 of UGT2B10 was substituted with histidine, and the capacity of the wild-type and mutant proteins to glucuronidate 4MU, 1NP, LTG, TFP, and naproxen was characterized.	Histidine	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19487247-5	2009	The conserved N-terminal domain histidine of UGT1A1, UGT1A6, UGT1A9, and UGT2B7 was mutated to proline and leucine 34 of UGT2B10 was substituted with histidine, and the capacity of the wild-type and mutant proteins to glucuronidate 4MU, 1NP, LTG, TFP, and naproxen was characterized.	Proline	95-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19541828-2	2009	The purpose of this study was to determine whether the genetic polymorphisms in the RNA polymerase II core promoter and the upstream phenobarbital-responsive element module (PBREM) of the UGT1A1 promoter have combined effects on UGT1A1 transcription mediated by the transcription factors.	Phenobarbital	133-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
19541828-2	2009	The purpose of this study was to determine whether the genetic polymorphisms in the RNA polymerase II core promoter and the upstream phenobarbital-responsive element module (PBREM) of the UGT1A1 promoter have combined effects on UGT1A1 transcription mediated by the transcription factors.	Phenobarbital	133-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	229-235
19487247-5	2009	The conserved N-terminal domain histidine of UGT1A1, UGT1A6, UGT1A9, and UGT2B7 was mutated to proline and leucine 34 of UGT2B10 was substituted with histidine, and the capacity of the wild-type and mutant proteins to glucuronidate 4MU, 1NP, LTG, TFP, and naproxen was characterized.	Leucine	107-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19487247-5	2009	The conserved N-terminal domain histidine of UGT1A1, UGT1A6, UGT1A9, and UGT2B7 was mutated to proline and leucine 34 of UGT2B10 was substituted with histidine, and the capacity of the wild-type and mutant proteins to glucuronidate 4MU, 1NP, LTG, TFP, and naproxen was characterized.	Histidine	150-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19487247-5	2009	The conserved N-terminal domain histidine of UGT1A1, UGT1A6, UGT1A9, and UGT2B7 was mutated to proline and leucine 34 of UGT2B10 was substituted with histidine, and the capacity of the wild-type and mutant proteins to glucuronidate 4MU, 1NP, LTG, TFP, and naproxen was characterized.	glucuronidate	218-231	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19486934-5	2009	It has been reported that UDP-glucuronosyltransferase (UGT) 1A1, UGT1A8, UGT1A9, and UGT1A10 are enzymes for raloxifene glucuronidation, and UGT1A8 and UGT1A10 are absent in the human liver, whereas UGT1A1, UGT1A8, UGT1A9, and UGT1A10 are present in the human intestine.	Raloxifene Hydrochloride	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-63
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	31-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	43-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	75-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-2	2009	However, significant interindividual pharmacokinetic variability in SN-38 is caused by factors, including inherited predispositions that may affect the function and expression of UGT1A1.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
19755821-4	2009	Similar to SN-38, bilirubin is excreted into bile after being glucuronidated by UGT1A1.	Bilirubin	18-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
20084161-8	2009	The US Food and Drug Administration has approved the UDP-glucuronosyltransferase 1A1 test in patients treated with irinotecan, and additional approval of newer tests is anticipated.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-84
19545173-2	2009	The results indicated that these isoflavones are metabolized most rapidly at three different concentrations by one of these four UGT isoforms: UGT1A1, UGT1A8, UGT1A9 and UGT1A10.	Isoflavones	33-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
19486253-1	2009	BACKGROUND AND AIMS: The gene product of the uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is crucial to bilirubin metabolism.	Bilirubin	117-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-93
19486253-1	2009	BACKGROUND AND AIMS: The gene product of the uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is crucial to bilirubin metabolism.	Bilirubin	117-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
19482841-6	2009	The effects of clinical factors and variants of the UGT1A1 gene on serum bilirubin levels were determined.	Bilirubin	73-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
20719167-4	2009	Irinotecan is also metabolized by carboxylesterase to its principal active metabolite, SN-38, which is subsequently glucuronidated by UGT1As to form the inactive compound SN-38G.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-138
20719167-4	2009	Irinotecan is also metabolized by carboxylesterase to its principal active metabolite, SN-38, which is subsequently glucuronidated by UGT1As to form the inactive compound SN-38G.	Irinotecan	87-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-138
20719167-4	2009	Irinotecan is also metabolized by carboxylesterase to its principal active metabolite, SN-38, which is subsequently glucuronidated by UGT1As to form the inactive compound SN-38G.	Irinotecan	171-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-138
20719167-5	2009	UGT1A1(*)28 and UGT1A1(*)6 polymorphisms were useful for predicting severe toxicity with NSCLC patients treated with irinotecan-based chemotherapy.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
20719167-5	2009	UGT1A1(*)28 and UGT1A1(*)6 polymorphisms were useful for predicting severe toxicity with NSCLC patients treated with irinotecan-based chemotherapy.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
19486934-5	2009	It has been reported that UDP-glucuronosyltransferase (UGT) 1A1, UGT1A8, UGT1A9, and UGT1A10 are enzymes for raloxifene glucuronidation, and UGT1A8 and UGT1A10 are absent in the human liver, whereas UGT1A1, UGT1A8, UGT1A9, and UGT1A10 are present in the human intestine.	Raloxifene Hydrochloride	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
19372226-8	2009	Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1.	Imipramine	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
19406951-0	2009	Characterizing the effects of common UDP glucuronosyltransferase (UGT) 1A6 and UGT1A1 polymorphisms on cis- and trans-resveratrol glucuronidation.	Resveratrol	112-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
19339377-9	2009	Further oxidation to THC-COOH surprisingly leads to a loss in metabolism by UGT1A9 and UGT1A10, while creating a substrate recognized by UGT1A1 and UGT1A3.	Dronabinol	21-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
19414484-3	2009	Meta-analysis showed strong replication for a genetic influence on serum bilirubin levels of the UGT1A1 locus (P &lt; 5 x 10(-324)) and a 12p12.2 locus.	Bilirubin	73-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
19414484-6	2009	The top variants in UGT1A1 and SLCO1B1 explain approximately 18.0 and approximately 1.0% of the variation in total serum bilirubin levels, respectively.	Bilirubin	121-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
19414484-8	2009	In one of the largest genetic studies of bilirubin to date (n = 9464), we confirm the substantial genetic influence of UGT1A1 variants, consistent with past linkage and association studies, and additionally provide strong evidence of a role for allelic variation in SLCO1B1.	Bilirubin	41-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
19414484-10	2009	In analyses for association with gallbladder disease or gallstones, top bilirubin SNPs in UGT1A1 and SLCO1B1 were not associated.	Bilirubin	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
19419973-5	2009	In addition to the two known loci previously involved in the regulation of bilirubin levels, UGT1A1 (P = 6.2 x 10(-62)) and G6PD (P = 2.5 x 10(-8)), we observed a strong association on chromosome 12 within the SLCO1B3 gene (P = 3.9 x 10(-9)).	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
19397531-5	2009	In the hyperbilirubinemic group, 23 of 91 (25.3%) infants demonstrated variant of UGT1A1 at nucleotides (nt) 211 as compared to 6 of 86 (7%) in the control group (p = 0.001).	Nucleotides	54-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
19841506-4	2009	Of note, both patients recovered from their initial unconjugated hyperbilirubinemia despite continuation of ribavirin therapy, which indicates that compensatory mechanisms leading to a normalization of UGT1A1 activity are likely.	Ribavirin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	202-208
19339377-9	2009	Further oxidation to THC-COOH surprisingly leads to a loss in metabolism by UGT1A9 and UGT1A10, while creating a substrate recognized by UGT1A1 and UGT1A3.	Carbonic Acid	25-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
19372226-8	2009	Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
19372226-8	2009	Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1.	Nitrogen	220-221	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
19372226-8	2009	Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1.	motesanib diphosphate	241-250	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
19409404-6	2009	Differentially expressed genes included the Phase I xenobiotic, fatty acid, sterol and steroid metabolism genes Cyp2b2 and CYP2B6, Cyp3a1 and CYP3A4, and Cyp4a22 and CYP4A11; Phase II conjugation enzyme genes Ugt1a1 and UGT1A1; and Phase III ABC transporter genes Abcb1 and ABCB1.	Sterols	76-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
19620808-1	2009	Severe neutropenia attributable to irinotecan hydrochloride (CPT-11) is reportedly associated with gene polymorphism of UGT1A1 related to its metabolism.	Irinotecan	35-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
19620808-1	2009	Severe neutropenia attributable to irinotecan hydrochloride (CPT-11) is reportedly associated with gene polymorphism of UGT1A1 related to its metabolism.	Irinotecan	61-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
19620808-9	2009	Nine days following administration of the first course, we found neutropenia of grade 3 and a fever of 38 degrees C. Analysis of the UGT1A1 gene polymorphism after symptom improvement revealed UGT1A1(*)28 homozygosity in both cases, which suggests that when FOLFIRI is conducted on a patient with homozygous UGT1A1(*)28, it is necessary to pay attention to neutropenia even with a CPT-11 dosage of 120 mg/m(2).	Irinotecan	381-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
19620808-9	2009	Nine days following administration of the first course, we found neutropenia of grade 3 and a fever of 38 degrees C. Analysis of the UGT1A1 gene polymorphism after symptom improvement revealed UGT1A1(*)28 homozygosity in both cases, which suggests that when FOLFIRI is conducted on a patient with homozygous UGT1A1(*)28, it is necessary to pay attention to neutropenia even with a CPT-11 dosage of 120 mg/m(2).	Irinotecan	381-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	193-199
19620808-9	2009	Nine days following administration of the first course, we found neutropenia of grade 3 and a fever of 38 degrees C. Analysis of the UGT1A1 gene polymorphism after symptom improvement revealed UGT1A1(*)28 homozygosity in both cases, which suggests that when FOLFIRI is conducted on a patient with homozygous UGT1A1(*)28, it is necessary to pay attention to neutropenia even with a CPT-11 dosage of 120 mg/m(2).	Irinotecan	381-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	193-199
19513514-14	2009	However, significant genotypic variation of UGT1A1, which was assumed to affect irinotecan toxicity, was not observed to affect RR, toxicity or survival.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
19409404-6	2009	Differentially expressed genes included the Phase I xenobiotic, fatty acid, sterol and steroid metabolism genes Cyp2b2 and CYP2B6, Cyp3a1 and CYP3A4, and Cyp4a22 and CYP4A11; Phase II conjugation enzyme genes Ugt1a1 and UGT1A1; and Phase III ABC transporter genes Abcb1 and ABCB1.	Sterols	76-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	220-226
19409404-6	2009	Differentially expressed genes included the Phase I xenobiotic, fatty acid, sterol and steroid metabolism genes Cyp2b2 and CYP2B6, Cyp3a1 and CYP3A4, and Cyp4a22 and CYP4A11; Phase II conjugation enzyme genes Ugt1a1 and UGT1A1; and Phase III ABC transporter genes Abcb1 and ABCB1.	Steroids	87-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
19409404-6	2009	Differentially expressed genes included the Phase I xenobiotic, fatty acid, sterol and steroid metabolism genes Cyp2b2 and CYP2B6, Cyp3a1 and CYP3A4, and Cyp4a22 and CYP4A11; Phase II conjugation enzyme genes Ugt1a1 and UGT1A1; and Phase III ABC transporter genes Abcb1 and ABCB1.	Steroids	87-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	220-226
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
19279563-6	2009	Plasma concentrations of raltegravir are modestly higher in individuals with the UGT1A1*28/*28 genotype than in those with the UGT1A1*1/*1 genotype.	Raltegravir Potassium	25-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
19349540-1	2009	PURPOSE: We aim to identify genetic variation, in addition to the UGT1A1*28 polymorphism, that can explain the variability in irinotecan (CPT-11) pharmacokinetics and neutropenia in cancer patients.	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
19349540-1	2009	PURPOSE: We aim to identify genetic variation, in addition to the UGT1A1*28 polymorphism, that can explain the variability in irinotecan (CPT-11) pharmacokinetics and neutropenia in cancer patients.	Irinotecan	138-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	33-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
19279563-0	2009	Pharmacokinetics of raltegravir in individuals with UGT1A1 polymorphisms.	Raltegravir Potassium	20-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
19279563-1	2009	Raltegravir is a human immunodeficiency virus-1 (HIV-1) integrase strand transfer inhibitor metabolized by glucuronidation via UDP-glucuronosyltransferase 1A1 (UGT1A1).	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
19279563-4	2009	The geometric mean ratio (GMR) (UGT1A1*28/*28 to UGT1A1*1/*1) and 90% confidence interval (CI) were 1.41 (0.96, 2.09) for raltegravir area under the concentration-time curve (AUC(0-infinity)), 1.40 (0.86, 2.28) for maximum plasma concentration (C(max)), and 1.91 (1.43, 2.55) for concentration at the 12-h time point (C(12 h)).	Raltegravir Potassium	122-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
19279563-4	2009	The geometric mean ratio (GMR) (UGT1A1*28/*28 to UGT1A1*1/*1) and 90% confidence interval (CI) were 1.41 (0.96, 2.09) for raltegravir area under the concentration-time curve (AUC(0-infinity)), 1.40 (0.86, 2.28) for maximum plasma concentration (C(max)), and 1.91 (1.43, 2.55) for concentration at the 12-h time point (C(12 h)).	Raltegravir Potassium	122-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
19279563-6	2009	Plasma concentrations of raltegravir are modestly higher in individuals with the UGT1A1*28/*28 genotype than in those with the UGT1A1*1/*1 genotype.	Raltegravir Potassium	25-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
19251824-5	2009	In HepG2 and LS180 cells stably transduced with PXR.1, PXR target genes (CYP3A4, MDR1, CYP2B6, and UGT1A1) were higher than mock-transduced cells in the absence of ligand and were further induced in the presence of rifampin.	Rifampin	215-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
19343046-7	2009	Results of linear multiple regression analysis on serum total bilirubin levels followed by analysis of variance showed that at least 13% of the variance in serum total bilirubin levels could be explained by three haplotype-tagging SNPs in the UGT1A1 gene.	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
19336732-0	2009	Cruciferous vegetable feeding alters UGT1A1 activity: diet- and genotype-dependent changes in serum bilirubin in a controlled feeding trial.	Bilirubin	100-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
19343046-2	2009	On analysis, we observed a strong association between five SNPs within the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene and serum total bilirubin levels (minimum P-value in Mann-Whitney test=1.82 x 10(10)).	Bilirubin	153-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-122
19343046-2	2009	On analysis, we observed a strong association between five SNPs within the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene and serum total bilirubin levels (minimum P-value in Mann-Whitney test=1.82 x 10(10)).	Bilirubin	153-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
19343046-3	2009	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid, thus enhancing bilirubin elimination.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19343046-3	2009	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid, thus enhancing bilirubin elimination.	Glucuronic Acid	51-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19343046-3	2009	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid, thus enhancing bilirubin elimination.	Bilirubin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19343046-7	2009	Results of linear multiple regression analysis on serum total bilirubin levels followed by analysis of variance showed that at least 13% of the variance in serum total bilirubin levels could be explained by three haplotype-tagging SNPs in the UGT1A1 gene.	Bilirubin	168-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
19364970-1	2009	PURPOSE: UGT1A1*28 is considered the main pharmacogenetic predictor of the toxicity outcome of irinotecan-treated patients.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
19223645-2	2009	Raltegravir is primarily cleared by hepatic metabolism via glucuronidation (via UDP glucuronosyltransferase 1A1), with a minor component of elimination occurring via the renal pathway.	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-111
18998132-0	2009	Life-threatening toxicities in a patient with UGT1A1*6/*28 and SLCO1B1*15/*15 genotypes after irinotecan-based chemotherapy.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18998132-6	2009	CONCLUSION: The severe toxicities in this patient are attributable to the extensive accumulation of SN-38, which may result from a synergistic or additive effect of low metabolic (UGT1A1*6/*28) and transport (SLCO1B1*15/*15) capabilities.	Irinotecan	100-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
19303655-4	2009	Indinavir (IDV) can lead to hyperbilirubinemia in Gilbert"s syndrome (UGT1A1*28), which does not explain interindividual severity differences and may thus involve additional UGT1A variants.	Indinavir	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
19364970-10	2009	CONCLUSION: We propose that UGT1A variants additional to UGT1A1*28 might improve the prediction of the outcome of colorectal cancer patients treated with FOLFIRI.	FOLFIRI regimen	154-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
19207584-0	2009	UGT1A1 gene polymorphism as a potential factor inducing iron overload in the pathogenesis of type 1 hereditary hemochromatosis.	Iron	56-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19207584-6	2009	Results High incidence and a significant correlation of UGT1A1 gene mutations with increased serum bilirubin level and lower grades of liver tissue inflammatory activity were observed in study participants.	Bilirubin	99-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
19207584-9	2009	Conclusions UGT1A1 gene polymorphism and as its consequence of high serum bilirubin level may promote iron accumulation in hemochromatosis patients by reducing the activity of inflammation.	Bilirubin	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
19207584-9	2009	Conclusions UGT1A1 gene polymorphism and as its consequence of high serum bilirubin level may promote iron accumulation in hemochromatosis patients by reducing the activity of inflammation.	Iron	102-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
19450125-0	2009	UGT1A1*28 genotype predicts gastrointestinal toxicity in patients treated with intermediate-dose irinotecan.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19450125-1	2009	AIMS: Variants in UGT1A1 have previously been associated with toxicity from irinotecan chemotherapy.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
19450125-2	2009	We conducted a pragmatic prospective cohort study to establish the relevance of UGT1A1 variants in the prediction of severe diarrhea and neutropenia in patients with colorectal cancer receiving irinotecan in a routine clinical setting.	Irinotecan	194-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
19371317-0	2009	Effects of UGT1A1*28 polymorphism on raloxifene pharmacokinetics and pharmacodynamics.	Raloxifene Hydrochloride	37-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
19371317-2	2009	Bilirubin is a typical UGT1A1 substrate.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
19371317-3	2009	Based on these facts, we postulated a hypothesis that UGT1A1 is the key enzyme for metabolic clearance of raloxifene and that the common UGT1A1*28 polymorphism significantly contributes to the large pharmacokinetic variability of raloxifene.	Raloxifene Hydrochloride	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
19371317-3	2009	Based on these facts, we postulated a hypothesis that UGT1A1 is the key enzyme for metabolic clearance of raloxifene and that the common UGT1A1*28 polymorphism significantly contributes to the large pharmacokinetic variability of raloxifene.	Raloxifene Hydrochloride	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
19371317-3	2009	Based on these facts, we postulated a hypothesis that UGT1A1 is the key enzyme for metabolic clearance of raloxifene and that the common UGT1A1*28 polymorphism significantly contributes to the large pharmacokinetic variability of raloxifene.	Raloxifene Hydrochloride	230-240	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
19371317-10	2009	CONCLUSIONS: In this study it is shown that a relatively common UGT1A1*28 polymorphism may considerably influence raloxifene pharmacokinetics and pharmacodynamics.	Raloxifene Hydrochloride	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
19336732-2	2009	UGT1A1 glucuronidates bilirubin, estrogens, and several dietary carcinogens.	Bilirubin	22-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19034627-6	2009	Notably, the flavonoids induced the expression of UGT1A1 and CYP1A2 in HepG2 cells but not in HPH.	Flavonoids	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
19390945-0	2009	UGT1A1*6 polymorphism is most predictive of severe neutropenia induced by irinotecan in Japanese cancer patients.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19390945-1	2009	BACKGROUND: Gene polymorphisms of the UDP-glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) contribute to individual variations in adverse events among patients administered irinotecan, and the distribution of the polymorphisms shows large interethnic differences.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-90
19390945-1	2009	BACKGROUND: Gene polymorphisms of the UDP-glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) contribute to individual variations in adverse events among patients administered irinotecan, and the distribution of the polymorphisms shows large interethnic differences.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19390945-3	2009	In the present study, we evaluated the association of genetic polymorphisms of UGT1A1 and SLCO1B1 with irinotecanrelated neutropenia in Japanese cancer patients.	irinotecanrelated	103-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
19390945-12	2009	CONCLUSION: These findings suggest that the UGT1A1*6 polymorphism is a potential predictor of severe neutropenia caused by irinotecan in Japanese cancer patients.	Irinotecan	123-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
19601871-2	2009	The involvement of UGT 1A1, 1A3 and 2B7 in buprenorpine and 1A3 in norbuprenorphine glucuronidation were confirmed.	buprenorpine	43-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-26
19601871-2	2009	The involvement of UGT 1A1, 1A3 and 2B7 in buprenorpine and 1A3 in norbuprenorphine glucuronidation were confirmed.	norbuprenorphine	67-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-26
19034627-4	2009	RESULTS: In human primary hepatocytes, real-time PCR analysis showed induction of CYP2B6, CYP3A4, UGT1A1, MDR1, and MRP2 by EGb 761, ginkgolide A (GA) and ginkgolide B (GB), but not by bilobalide (BB) or the flavonoids (quercetin, kaempferol and tamarixetin) of GBE.	BDBM50323769	124-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
19268007-0	2009	Does bilirubin level correspond to interaction of c.-3279T&gt;G and A(TA)7TAA variants in UGT1A1 gene?	Bilirubin	5-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
19141701-0	2009	Citrus fruit intake is associated with lower serum bilirubin concentration among women with the UGT1A1*28 polymorphism.	Bilirubin	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
19141701-1	2009	UDP-glucuronosyltransferase (UGT) 1A1 glucuronidates bilirubin, estrogens, and xenobiotic compounds.	Bilirubin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
19141701-2	2009	The UGT1A1*28 polymorphism results in lower promoter activity due to 7 thymine-adenine (TA) repeats rather than the more common 6 TA repeats.	7 thymine-adenine	69-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19141701-2	2009	The UGT1A1*28 polymorphism results in lower promoter activity due to 7 thymine-adenine (TA) repeats rather than the more common 6 TA repeats.	Tantalum	88-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19141701-3	2009	Previously, we showed that serum bilirubin, a marker of UGT1A1 activity, was lower among individuals homozygous for the UGT1A1*28 polymorphism (7/7) when randomized to a high fruit and vegetable (F&amp;V) diet, whereas there was no effect in individuals with the wild-type (6/6) and heterozygous (6/7) genotypes.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
19141701-3	2009	Previously, we showed that serum bilirubin, a marker of UGT1A1 activity, was lower among individuals homozygous for the UGT1A1*28 polymorphism (7/7) when randomized to a high fruit and vegetable (F&amp;V) diet, whereas there was no effect in individuals with the wild-type (6/6) and heterozygous (6/7) genotypes.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
19268007-1	2009	Promoter variants c.-3279T&gt;G and A(TA)7TAA show decreased level of expression of UDP-glucuronosyl transferase 1A1 (UGT1A1) and consequently reduced activity of the enzyme catalyzing glucuronidation of bilirubin in hepatocytes.	Bilirubin	204-213	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-116
19268007-1	2009	Promoter variants c.-3279T&gt;G and A(TA)7TAA show decreased level of expression of UDP-glucuronosyl transferase 1A1 (UGT1A1) and consequently reduced activity of the enzyme catalyzing glucuronidation of bilirubin in hepatocytes.	Bilirubin	204-213	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
18685565-0	2009	Phase I/II pharmacokinetic and pharmacogenomic study of UGT1A1 polymorphism in elderly patients with advanced non-small cell lung cancer treated with irinotecan.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
18685565-9	2009	An analysis of the influence of UGT1A1*28 and *6 polymorphisms provides useful information for the prediction of CPT-11-related hematological toxicity.	Irinotecan	113-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
19571434-10	2009	In the present study, Kampo was clarified to inhibit beta-estradiol and SN-38 glucuronidation mainly catalyzed by UGT1A1.	Estradiol	53-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
19414151-4	2009	UGT1A1*28 leads to reduced conjugation of SN-38, the active metabolite of irinotecan, resulting in an increased rate of adverse effects, especially neutropenia.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19414151-4	2009	UGT1A1*28 leads to reduced conjugation of SN-38, the active metabolite of irinotecan, resulting in an increased rate of adverse effects, especially neutropenia.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18981166-0	2009	Close association of UGT1A9 IVS1+399C&gt;T with UGT1A1*28, *6, or *60 haplotype and its apparent influence on 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation in Japanese.	Irinotecan	142-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	68-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	100-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	133-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-11	2009	Thus, at least in Japanese populations, influence of I399C&gt;T on SN-38 glucuronidation is attributable to its close association with either UGT1A1*6, *28, or *60.	Irinotecan	67-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
19571434-10	2009	In the present study, Kampo was clarified to inhibit beta-estradiol and SN-38 glucuronidation mainly catalyzed by UGT1A1.	Irinotecan	72-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
20045987-9	2009	These results suggest that glycyrrhetinic acid glucuronidation is primarily mediated by UGT1A1, 1A3, 2B4 and 2B7.	Glycyrrhetinic Acid	27-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
18221820-5	2009	The UGT1A1*6/*6, UGT1A9*1/*1 or *1/*22, and SLCO1B1 521TC or CC genotypes, and female-gender were predictive for higher AUC(SN-38) in multivariate analysis.	Irinotecan	124-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19125128-0	2009	Recommendations from the EGAPP Working Group: can UGT1A1 genotyping reduce morbidity and mortality in patients with metastatic colorectal cancer treated with irinotecan?	Irinotecan	158-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
19125128-8	2009	CLINICAL VALIDITY: The EWG found adequate evidence of a significant association between UGT1A1 genotype and the incidence of severe neutropenia at standard doses of irinotecan.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
19125128-16	2009	Further rigorous evaluation of UGT1A1 genotyping using current and promising irinotecan treatment protocols is warranted.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
19125129-0	2009	Can UGT1A1 genotyping reduce morbidity and mortality in patients with metastatic colorectal cancer treated with irinotecan?	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19125129-2	2009	This evidence-based review addresses the question of whether testing for UGT1A1 mutations in patients with metastatic colorectal cancer treated with irinotecan leads to improvement in outcomes (e.g., irinotecan toxicity, response to treatment, morbidity, and mortality), when compared with no testing.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19125129-2	2009	This evidence-based review addresses the question of whether testing for UGT1A1 mutations in patients with metastatic colorectal cancer treated with irinotecan leads to improvement in outcomes (e.g., irinotecan toxicity, response to treatment, morbidity, and mortality), when compared with no testing.	Irinotecan	200-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19125129-16	2009	Given the large number of colorectal cancer cases diagnosed each year, a randomized controlled trial of the effects of irinotecan dose modifications in patients with colorectal cancer based on their UGT1A1 genotype is feasible and could clarify the tradeoffs between possible reductions in severe neutropenia and improved tumor response and/or survival in patients with various UGT1A1 genotypes.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
19125129-16	2009	Given the large number of colorectal cancer cases diagnosed each year, a randomized controlled trial of the effects of irinotecan dose modifications in patients with colorectal cancer based on their UGT1A1 genotype is feasible and could clarify the tradeoffs between possible reductions in severe neutropenia and improved tumor response and/or survival in patients with various UGT1A1 genotypes.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	378-384
19356098-0	2008	Induction of human UGT1A1 by bilirubin through AhR dependent pathway.	Bilirubin	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
19325249-1	2009	BACKGROUND: The uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) enzyme is responsible for conjugation of the bilirubin in the liver as well as for drug metabolism.	Bilirubin	118-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-63
19325249-1	2009	BACKGROUND: The uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) enzyme is responsible for conjugation of the bilirubin in the liver as well as for drug metabolism.	Bilirubin	118-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
19299905-0	2009	Clinical significance of UDP-glucuronosyltransferase 1A1*6 for toxicities of combination chemotherapy with irinotecan and cisplatin in gynecologic cancers: a prospective multi-institutional study.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-56
19299905-0	2009	Clinical significance of UDP-glucuronosyltransferase 1A1*6 for toxicities of combination chemotherapy with irinotecan and cisplatin in gynecologic cancers: a prospective multi-institutional study.	Cisplatin	122-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-56
19299905-1	2009	BACKGROUND: To investigate the effects of UDP-glucuronosyltransferase 1A1 (UGT1A1) *28, *6 and *27 in patients with gynecologic cancer who received chemotherapy with irinotecan and cisplatin.	Irinotecan	166-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-73
19299905-9	2009	CONCLUSION: In addition to UGT1A1*28, UGT1A1*6 might also be a key candidate to determine the dose of combination chemotherapy with irinotecan and cisplatin.	Irinotecan	132-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
19299905-9	2009	CONCLUSION: In addition to UGT1A1*28, UGT1A1*6 might also be a key candidate to determine the dose of combination chemotherapy with irinotecan and cisplatin.	Cisplatin	147-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
18953066-0	2008	Genetic testing for UGT1A1*28 and *6 in Japanese patients who receive irinotecan chemotherapy.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
19059062-3	2008	Irinotecan toxicity in patients who have colorectal cancer has been linked to reduced activity of uridine diphosphate-glucuronyltransferase 1A1 (UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-143
19059062-3	2008	Irinotecan toxicity in patients who have colorectal cancer has been linked to reduced activity of uridine diphosphate-glucuronyltransferase 1A1 (UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
19356098-2	2008	In this report, we show findings of the induction of the reporter gene (-3475/+14) of UGT1A1 in HepG2 cells by bilirubin at 50 microM, 100 microM, with human aryl hydrocarbon receptor (hAhR).	Bilirubin	111-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
19712005-3	2009	METHODS: Here, we assess the genome of 469 individuals from Sao Miguel Island (Azores, Portugal) in order to determine the frequencies of polymorphisms and haplotypes in UGT1A1, UGT1A6, and UGT1A7, the co-occurrence of reduced enzyme activity UGT1A variants related to irinotecan toxicity, and to calculate the extent of linkage disequilibrium (LD) in the genomic region encompassing these genes.	Irinotecan	269-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
19639031-6	2008	UGT1A1 genotype added approximately 8-9% during cycle 1 and from approximately 7% [mIFL regimen] to 26% [CapeIRI regimen] after cycle 1.	capeiri	105-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18990428-3	2008	BPA glucuronidation was catalyzed by UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7 and UGT2B15 as well as by human liver microsomes.	bisphenol A	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
18528434-1	2008	Atazanavir (ATV) is known to inhibit UGT1A1-mediated glucuronidation.	Atazanavir Sulfate	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
18528434-1	2008	Atazanavir (ATV) is known to inhibit UGT1A1-mediated glucuronidation.	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
19356098-1	2008	UDP-glucuronosyltransferase1A1 (UGT1A1) plays a key role to conjugate bilirubin and preventing jaundice, but there is no report showing the induction of human UGT1A1 (UGT1A1) by bilirubin.	Bilirubin	70-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
19356098-1	2008	UDP-glucuronosyltransferase1A1 (UGT1A1) plays a key role to conjugate bilirubin and preventing jaundice, but there is no report showing the induction of human UGT1A1 (UGT1A1) by bilirubin.	Bilirubin	70-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
19356098-1	2008	UDP-glucuronosyltransferase1A1 (UGT1A1) plays a key role to conjugate bilirubin and preventing jaundice, but there is no report showing the induction of human UGT1A1 (UGT1A1) by bilirubin.	Bilirubin	178-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
19356098-6	2008	These results indicate that the induction of UGT1A1 by bilirubin-AhR did not depend on the elevation of AhR but on ligand binding.	Bilirubin	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
19356098-7	2008	From this result, we considered that high bilirubin in neonates must induce the elevation of UGT1A1 after birth to prevent jaundice, and bilirubin in adults also regulates the level of UGT1A1.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
19356098-7	2008	From this result, we considered that high bilirubin in neonates must induce the elevation of UGT1A1 after birth to prevent jaundice, and bilirubin in adults also regulates the level of UGT1A1.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
19356098-7	2008	From this result, we considered that high bilirubin in neonates must induce the elevation of UGT1A1 after birth to prevent jaundice, and bilirubin in adults also regulates the level of UGT1A1.	Bilirubin	137-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
19356098-8	2008	This is the first report showing direct induction of UGT1A1 by a bilirubin through AhR pathway.	Bilirubin	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
18558463-5	2008	Also, elevated bilirubin levels, due to liver impairment, conjugation disorders or UGT1A1 *28 genotype, have been associated with increased incidence of grades 3 intestinal toxicity and neutropenia.	Bilirubin	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
18335219-0	2008	Cisplatin plus weekly CPT-11/docetaxel in advanced esophagogastric cancer: a phase I study with pharmacogenetic assessment of XPD, XRCC3 and UGT1A1 polymorphisms.	Cisplatin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
18335219-1	2008	PURPOSE: A multicenter phase I trial to establish the recommended dose of CPT-11/docetaxel plus cisplatin in advanced esophagogastric cancer patients and to correlate the efficacy and toxicity with genetic polymorphisms in DNA repair genes (XPD and XRCC3) and the UGT1A1 gene.	Irinotecan	74-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
18790042-2	2008	UGT1A1 is the major gene influencing bilirubin concentrations.	Bilirubin	37-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18790042-3	2008	Therefore, we investigated an association of bilirubin levels and two polymorphisms in the promoter of UGT1A1 (-53(TA-repeat) polymorphism and T-3279G) in 477 patients with premature, familial CAD and 619 age- and sex-matched controls.	Bilirubin	45-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
18558463-6	2008	UGT1A1 *28 homozygosity is strongly associated with irinotecan-induced neutropenia and polymorphisms in the transporting peptides ABCB1 and OATP1B1 have also been associated with gastrointestinal toxicity and irinotecan pharmacokinetics, respectively.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18335219-1	2008	PURPOSE: A multicenter phase I trial to establish the recommended dose of CPT-11/docetaxel plus cisplatin in advanced esophagogastric cancer patients and to correlate the efficacy and toxicity with genetic polymorphisms in DNA repair genes (XPD and XRCC3) and the UGT1A1 gene.	Docetaxel	81-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
18558463-6	2008	UGT1A1 *28 homozygosity is strongly associated with irinotecan-induced neutropenia and polymorphisms in the transporting peptides ABCB1 and OATP1B1 have also been associated with gastrointestinal toxicity and irinotecan pharmacokinetics, respectively.	Irinotecan	209-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18558463-7	2008	In the irinotecan product label, it is advised to reduce the irinotecan starting dose for UGT1A1 *28 homozygotes.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
18558463-7	2008	In the irinotecan product label, it is advised to reduce the irinotecan starting dose for UGT1A1 *28 homozygotes.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
18832463-2	2008	The basis of the disorder is a 70% reduction in bilirubin glucuronidation catalyzed by the UDP-glucuronosyltransferase 1A1 (UGT1A1), which, in Caucasians, is the result of a homozygous TA insertion into the promoter region of the UGT1A1 gene (UGT1A1*28).	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-122
18832463-2	2008	The basis of the disorder is a 70% reduction in bilirubin glucuronidation catalyzed by the UDP-glucuronosyltransferase 1A1 (UGT1A1), which, in Caucasians, is the result of a homozygous TA insertion into the promoter region of the UGT1A1 gene (UGT1A1*28).	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
18832463-2	2008	The basis of the disorder is a 70% reduction in bilirubin glucuronidation catalyzed by the UDP-glucuronosyltransferase 1A1 (UGT1A1), which, in Caucasians, is the result of a homozygous TA insertion into the promoter region of the UGT1A1 gene (UGT1A1*28).	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
18832463-2	2008	The basis of the disorder is a 70% reduction in bilirubin glucuronidation catalyzed by the UDP-glucuronosyltransferase 1A1 (UGT1A1), which, in Caucasians, is the result of a homozygous TA insertion into the promoter region of the UGT1A1 gene (UGT1A1*28).	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
18832463-3	2008	Homozygous carriers of UGT1A1*28 as well as those with additional UGT1A variants can suffer from severe irinotecan toxicity or jaundice during treatment with the protease inhibitor atazanavir.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18430559-0	2008	Glucuronidation of the soyabean isoflavones genistein and daidzein by human liver is related to levels of UGT1A1 and UGT1A9 activity and alters isoflavone response in the MCF-7 human breast cancer cell line.	Isoflavones	32-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
18832463-3	2008	Homozygous carriers of UGT1A1*28 as well as those with additional UGT1A variants can suffer from severe irinotecan toxicity or jaundice during treatment with the protease inhibitor atazanavir.	Atazanavir Sulfate	181-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18430559-0	2008	Glucuronidation of the soyabean isoflavones genistein and daidzein by human liver is related to levels of UGT1A1 and UGT1A9 activity and alters isoflavone response in the MCF-7 human breast cancer cell line.	Genistein	44-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
18634814-5	2008	Genistein, on the other hand, inhibited ST1E1 and UGT1A1 expressions, and led to 17beta-estradiol cellular retention.	Genistein	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
18430559-0	2008	Glucuronidation of the soyabean isoflavones genistein and daidzein by human liver is related to levels of UGT1A1 and UGT1A9 activity and alters isoflavone response in the MCF-7 human breast cancer cell line.	daidzein	58-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
18430559-0	2008	Glucuronidation of the soyabean isoflavones genistein and daidzein by human liver is related to levels of UGT1A1 and UGT1A9 activity and alters isoflavone response in the MCF-7 human breast cancer cell line.	Isoflavones	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
18430559-2	2008	We observed a correlation between rates of metabolism of marker substrates of specific UGTs and rates of glucuronidation of genistein and daidzein in vitro by a panel of human liver microsomes, demonstrating that UGT1A1 and UGT1A9, but not UGT1A4, make a major contribution to the metabolism of these isoflavones by human liver.	daidzein	138-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	213-219
18430559-2	2008	We observed a correlation between rates of metabolism of marker substrates of specific UGTs and rates of glucuronidation of genistein and daidzein in vitro by a panel of human liver microsomes, demonstrating that UGT1A1 and UGT1A9, but not UGT1A4, make a major contribution to the metabolism of these isoflavones by human liver.	Isoflavones	301-312	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	213-219
18430559-3	2008	These findings were substantiated by observations that recombinant human UGT1A1 and UGT1A9, but not UGT1A4, catalysed the production of the major glucuronides of both genistein and daidzein in vitro.	Glucuronides	146-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
18430559-3	2008	These findings were substantiated by observations that recombinant human UGT1A1 and UGT1A9, but not UGT1A4, catalysed the production of the major glucuronides of both genistein and daidzein in vitro.	Genistein	167-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
18430559-3	2008	These findings were substantiated by observations that recombinant human UGT1A1 and UGT1A9, but not UGT1A4, catalysed the production of the major glucuronides of both genistein and daidzein in vitro.	daidzein	181-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
18430559-7	2008	In view of a well-characterised functional polymorphism in UGT1A1, these observations may have implications for inter-individual variability in the potential health-beneficial effects of isoflavone consumption.	Isoflavones	187-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
18797458-2	2008	We included 49 patients treated for metastatic colorectal cancer with a combination of 5-fluorouracil and irinotecan; a polymorphism in the UGT1A1 gene (TA repeat in the TATA box) and one in the CES2 gene promoter (830C&gt;G) were studied as potential markers for SN-38 glucuronidation and irinotecan activation, respectively; and the potential activity of CYP3A4 was estimated from cortisol biotransformation into 6beta-hydroxycortisol.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
18797458-7	2008	The TATA box polymorphism of UGT1A1 was significantly associated with plasma bilirubin levels and behaved as a significant predictor for neutropoenia.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
18797458-10	2008	UGT1A1 genotyping plus cortisol 6beta-hydroxylation determination could help to determine the optimal dose of irinotecan.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18756540-4	2008	The UGT1A1 genotype significantly influenced average bilirubin levels for the common alleles: 6/6 genotype = 2.36 +/- 1.13 mg/dL, 6/7 genotype = 2.90 +/- 1.54 mg/dL, and 7/7 genotype = 4.24 +/- 2.11 mg/dL (P &lt; 0.0001).	Bilirubin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
18756540-8	2008	These results validate previous smaller studies and confirm that the UGT1A1 promoter polymorphism exerts a powerful influence on bilirubin levels and the development of gallbladder disease in children with SCA.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-141
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	325-331
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-141
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	325-331
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	213-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-141
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	325-331
18720361-2	2008	Individuals who are homozygous for the UGT1A1*28 allele (7 repeats) may exhibit reduced degradation of SN-38 and increased probability of severe toxicities.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
18720361-5	2008	Irinotecan labeling recommends testing for the UGT1A1*28 allele and reducing irinotecan dosing in patients who are positive to reduce the likelihood of dose-limiting neutropenia only, but not diarrhea.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
18675828-6	2008	Overall, UGT1A1-53 and -3156 genotypes modified the association between dietary benzo(a)pyrene (BaP) and colon cancer (P for interaction=0.02 and 0.03, respectively).	benzo(a)	80-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
18653743-5	2008	UGT1A1 and UGT1A9 were the major enzymes responsible for the formation of the most abundant conjugate, isoliquiritigenin 4"-O-glucuronide (MG5), with Km values of 4.30+/-0.47 and 3.15+/-0.24 microM, respectively.	isoliquiritigenin 4"-o-glucuronide	103-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18653743-5	2008	UGT1A1 and UGT1A9 were the major enzymes responsible for the formation of the most abundant conjugate, isoliquiritigenin 4"-O-glucuronide (MG5), with Km values of 4.30+/-0.47 and 3.15+/-0.24 microM, respectively.	3t83	139-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19014835-3	2008	The protease inhibitor atazanavir is a potent inhibitor of UGT1A1.	Atazanavir Sulfate	23-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
18653743-6	2008	UGT1A1 and UGT1A10 converted isoliquiritigenin to the next most abundant phase 2 metabolite, isoliquiritigenin 2"-O-glucuronide (MG4), with Km values of 2.98+/-0.8 and 25.8+/-1.3 microM, respectively.	isoliquiritigenin	29-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18653743-6	2008	UGT1A1 and UGT1A10 converted isoliquiritigenin to the next most abundant phase 2 metabolite, isoliquiritigenin 2"-O-glucuronide (MG4), with Km values of 2.98+/-0.8 and 25.8+/-1.3 microM, respectively.	isoliquiritigenin 2"-o-glucuronide	93-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18653743-6	2008	UGT1A1 and UGT1A10 converted isoliquiritigenin to the next most abundant phase 2 metabolite, isoliquiritigenin 2"-O-glucuronide (MG4), with Km values of 2.98+/-0.8 and 25.8+/-1.3 microM, respectively.	mg4	129-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18675828-6	2008	Overall, UGT1A1-53 and -3156 genotypes modified the association between dietary benzo(a)pyrene (BaP) and colon cancer (P for interaction=0.02 and 0.03, respectively).	pyrene	88-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
18675828-6	2008	Overall, UGT1A1-53 and -3156 genotypes modified the association between dietary benzo(a)pyrene (BaP) and colon cancer (P for interaction=0.02 and 0.03, respectively).	Benzo(a)pyrene	96-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
18675828-7	2008	The strongest association was observed for those with &lt;7.7 ng/day BaP exposure and the low activity genotypes, for both UGT1A1 28/28 (OR=1.8, 95% CI=1.1-2.9) and -3156AA (OR=1.7, 95% CI=1.0-3.0), compared to &gt;or=7.7 ng/day and combined high/intermediate genotypes.	Benzo(a)pyrene	69-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
18674515-13	2008	Kinetic analyses revealed that the main contributors to losartan glucuronidation in HLM are UGT1A1 and UGT2B7.	Losartan	56-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18594531-1	2008	The aim of the study was to investigate the associations between UGT1A1(*)28 genotype and (1) response rates, (2) febrile neutropenia and (3) dose intensity in patients with metastatic colorectal cancer treated with irinotecan.	Irinotecan	216-226	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
18781851-9	2008	Our results also demonstrate that possessing the *60/*60 plus *28/*28 diplotype in the UGT1A1 gene is a determinant of relatively higher bilirubin values amongst hyperbilirubinemic patients.	Bilirubin	137-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
18566038-12	2008	Preliminary in vitro phenotyping studies indicated that glucuronide formation is primarily catalyzed by UGT1A1, 1A3, and 1A9.	Glucuronides	56-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
17530442-0	2008	Induction of human UGT1A1 by a complex of dexamethasone-GR dependent on proximal site and independent of PBREM.	Dexamethasone	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
17530442-1	2008	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays a key role to conjugate bilirubin and prevent jaundice.	Bilirubin	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
17530442-1	2008	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays a key role to conjugate bilirubin and prevent jaundice.	Bilirubin	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
17530442-4	2008	In this report, we investigated the influence of PBREM on the induction of the UGT1A1 reporter gene by GR and PXR with dexamethasone (DEX).	Dexamethasone	119-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
17530442-4	2008	In this report, we investigated the influence of PBREM on the induction of the UGT1A1 reporter gene by GR and PXR with dexamethasone (DEX).	Dexamethasone	134-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
17530442-10	2008	This supports that hPXR induced UGT1A1 through PBREM by DEX.	Dexamethasone	56-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
17530442-11	2008	These results showed that PBREM has no relation with the induction by DEX-GR but the proximal site of UGT1A1 may function in stimulation by DEX-GR.	dex-gr	140-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
18594531-2	2008	UGT1A1(*)28 genotype was determined in 218 patients receiving irinotecan (either first-line therapy with capecitabine or second-line as monotherapy) for metastatic colorectal cancer.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18594531-2	2008	UGT1A1(*)28 genotype was determined in 218 patients receiving irinotecan (either first-line therapy with capecitabine or second-line as monotherapy) for metastatic colorectal cancer.	Capecitabine	105-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18503403-5	2008	By performing uridine diphosphate glucuronosyltransferase (UGT) 1A1 genetic testing, some studies have been able to predict which patients receiving irinotecan will experience the toxicity.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-67
18362158-3	2008	In this investigation we characterized the effects of albumin on the kinetics of 4-methylumbelliferone (4MU) glucuronidation by UDP-glucuronosyltransferase (UGT) 1A1, 1A6, and 1A9, and propofol (PRO) glucuronidation by UGT1A9 and HLM.	Hymecromone	81-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-165
18362158-3	2008	In this investigation we characterized the effects of albumin on the kinetics of 4-methylumbelliferone (4MU) glucuronidation by UDP-glucuronosyltransferase (UGT) 1A1, 1A6, and 1A9, and propofol (PRO) glucuronidation by UGT1A9 and HLM.	Hymecromone	104-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-165
18181169-4	2008	Independently, DHA and vitamin E resulted to affect only slightly UDP-glucuronosyltransferase 1A1 (UGT1A1) mRNA expression.	Docosahexaenoic Acids	15-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-97
18181169-4	2008	Independently, DHA and vitamin E resulted to affect only slightly UDP-glucuronosyltransferase 1A1 (UGT1A1) mRNA expression.	Docosahexaenoic Acids	15-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
18181169-4	2008	Independently, DHA and vitamin E resulted to affect only slightly UDP-glucuronosyltransferase 1A1 (UGT1A1) mRNA expression.	Vitamin E	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-97
18181169-4	2008	Independently, DHA and vitamin E resulted to affect only slightly UDP-glucuronosyltransferase 1A1 (UGT1A1) mRNA expression.	Vitamin E	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
18172616-1	2008	Human UDP-glucuronosyltransferase (UGT)1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds, such as potentially neurotoxic bilirubin and the anticancer drug irinotecan SN-38, via conjugation with glucuronic acid.	Bilirubin	191-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-42
18172616-1	2008	Human UDP-glucuronosyltransferase (UGT)1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds, such as potentially neurotoxic bilirubin and the anticancer drug irinotecan SN-38, via conjugation with glucuronic acid.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-42
18172616-1	2008	Human UDP-glucuronosyltransferase (UGT)1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds, such as potentially neurotoxic bilirubin and the anticancer drug irinotecan SN-38, via conjugation with glucuronic acid.	Irinotecan	236-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-42
18172616-1	2008	Human UDP-glucuronosyltransferase (UGT)1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds, such as potentially neurotoxic bilirubin and the anticancer drug irinotecan SN-38, via conjugation with glucuronic acid.	Glucuronic Acid	264-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-42
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
17700594-1	2008	Genetic polymorphisms in hepatically expressed UGT1A1 and UGT1A9 contribute to the interindividual variability i-n irinotecan disposition and toxicity.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
17700594-5	2008	UGT1A1-1A9 diplotype analysis showed that patients harbouring the H1/H2 (TG6GT(10)T/GG6GT(9)C) diplotype had 2.4-fold lower systemic exposure to SN-38 glucuronide (SN-38G) compared with patients harbouring the H1/H5 (TG6GT(10)T/GG6GT(10)C) diplotype (P=0.025).	7-ethyl-10-hydroxycamptothecin glucuronide	145-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17700594-5	2008	UGT1A1-1A9 diplotype analysis showed that patients harbouring the H1/H2 (TG6GT(10)T/GG6GT(9)C) diplotype had 2.4-fold lower systemic exposure to SN-38 glucuronide (SN-38G) compared with patients harbouring the H1/H5 (TG6GT(10)T/GG6GT(10)C) diplotype (P=0.025).	Irinotecan	145-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18633245-0	2008	[Role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction].	Irinotecan	36-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
18633245-0	2008	[Role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction].	Irinotecan	36-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18633245-3	2008	Irinotecan is metabolized by carboxylesterase to form an active metabolite, 7-ethyl-10-hydroxycamptothecin(SN-38), which in turn is subsequently conjugated by UGT-glucuronosyltransferase 1A1(UGT1A1)to yield an inactive form, SN-38 glucuronide(SN-38 G).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
18633245-3	2008	Irinotecan is metabolized by carboxylesterase to form an active metabolite, 7-ethyl-10-hydroxycamptothecin(SN-38), which in turn is subsequently conjugated by UGT-glucuronosyltransferase 1A1(UGT1A1)to yield an inactive form, SN-38 glucuronide(SN-38 G).	Irinotecan	76-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
18633245-3	2008	Irinotecan is metabolized by carboxylesterase to form an active metabolite, 7-ethyl-10-hydroxycamptothecin(SN-38), which in turn is subsequently conjugated by UGT-glucuronosyltransferase 1A1(UGT1A1)to yield an inactive form, SN-38 glucuronide(SN-38 G).	Irinotecan	107-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
18633245-4	2008	The UGT1A1 gene polymorphisms contribute to the individual variation in adverse events among patients administered irinotecan.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
18633245-7	2008	Recently, it has been demonstrated that genetic variants of UGT1A1*6 in addition to UGT1A1*28 are associated with the occurrence of adverse events in irinotecan chemotherapy in Asians.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
18633245-7	2008	Recently, it has been demonstrated that genetic variants of UGT1A1*6 in addition to UGT1A1*28 are associated with the occurrence of adverse events in irinotecan chemotherapy in Asians.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
18633245-8	2008	This review summarizes recent studies to outline the role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction in Japanese cancer patients.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
18633245-8	2008	This review summarizes recent studies to outline the role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction in Japanese cancer patients.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
18558634-5	2008	RESULTS: Genetic polymorphisms of the UGT1A1 promoter, specifically the T-3279G phenobarbital responsive enhancer module and the (thymidine-adenine)(7) dinucleotide repeat TATAA box variants, were common.	Phenobarbital	80-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
18362158-0	2008	The "albumin effect" and drug glucuronidation: bovine serum albumin and fatty acid-free human serum albumin enhance the glucuronidation of UDP-glucuronosyltransferase (UGT) 1A9 substrates but not UGT1A1 and UGT1A6 activities.	Fatty Acids	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
18633225-1	2008	We encountered a 64-year-old UGT1A1*28 heterotype patient who received CPT-11 and CDDP chemotherapy for Stage III A small-cell lung-cancer and developed grade 4 neutropenia as assessed by CTCAE v3.0 in Pharmaceutical Management.	Irinotecan	71-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
18633225-1	2008	We encountered a 64-year-old UGT1A1*28 heterotype patient who received CPT-11 and CDDP chemotherapy for Stage III A small-cell lung-cancer and developed grade 4 neutropenia as assessed by CTCAE v3.0 in Pharmaceutical Management.	cddp	82-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	277-283
18172616-6	2008	Thus, UGT1A1 gene promoter variations, including the TA repeat polymorphism and T-3279G gtPBREM, have important clinical implications.	gtpbrem	88-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
18466101-0	2008	Cost-effectiveness of UGT1A1 genotyping in second-line, high-dose, once every 3 weeks irinotecan monotherapy treatment of colorectal cancer.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
18541046-12	2008	We also estimates the potential effects of genetic variations: the AUC and Cmax of SN-38 may increase to 208% and 165% respectively with the genetic variation UGT1A1*28/*28 which reduces the expression of UGT1A1 down to 30%.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
18541046-12	2008	We also estimates the potential effects of genetic variations: the AUC and Cmax of SN-38 may increase to 208% and 165% respectively with the genetic variation UGT1A1*28/*28 which reduces the expression of UGT1A1 down to 30%.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	205-211
18343383-0	2008	Gilbert syndrome, UGT1A1*28 allele, and cardiovascular disease risk: possible protective effects and therapeutic applications of bilirubin.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
18343383-5	2008	HO and biliverdin reductase control the formation of bilirubin, whereas UGT1A1 controls bilirubin conjugation and clearance.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
18300238-0	2008	UGT1A1*28 polymorphism predicts irinotecan-induced severe toxicities without affecting treatment outcome and survival in patients with metastatic colorectal carcinoma.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18300238-1	2008	BACKGROUND: It is known that the uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1)*28 polymorphism reduces UGT1A1 enzyme activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-78
18300238-1	2008	BACKGROUND: It is known that the uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1)*28 polymorphism reduces UGT1A1 enzyme activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
18300238-1	2008	BACKGROUND: It is known that the uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1)*28 polymorphism reduces UGT1A1 enzyme activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
18300238-11	2008	CONCLUSIONS: The current data suggested that the UGT1A1*28 polymorphism may be a key determinant for predicting irinotecan-induced severe toxicities without affecting treatment outcome for patients with metastatic CRC.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
18375480-0	2008	Association between the UGT1A1 TA-repeat polymorphism and bilirubin concentration in patients with intermittent claudication: results from the CAVASIC study.	Bilirubin	58-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
18375480-2	2008	Low plasma concentrations of bilirubin are reportedly associated with the development of coronary and cerebrovascular disease, and bilirubin concentrations are strongly correlated with the enzyme activity of the hepatic uridine diphosphate glucuronosyltransferase (UGT1A1).	Bilirubin	131-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	265-271
18375480-4	2008	In a case-control study, we investigated the association between the UGT1A1 polymorphism, bilirubin concentration, and intermittent claudication.	Bilirubin	90-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
19372981-6	2008	Some other important advances in our knowledge have also been made, such as the association of TA repeats in the UGT1A1 regulatory region (UGT1A1 28) with atazanavir-related hyperbilirubinaemia and the association of ABCC2 and ABCC4 single nucleotide polymorphisms with tenofovir-associated renal toxicity.	Atazanavir Sulfate	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
19372981-6	2008	Some other important advances in our knowledge have also been made, such as the association of TA repeats in the UGT1A1 regulatory region (UGT1A1 28) with atazanavir-related hyperbilirubinaemia and the association of ABCC2 and ABCC4 single nucleotide polymorphisms with tenofovir-associated renal toxicity.	Atazanavir Sulfate	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
19372981-6	2008	Some other important advances in our knowledge have also been made, such as the association of TA repeats in the UGT1A1 regulatory region (UGT1A1 28) with atazanavir-related hyperbilirubinaemia and the association of ABCC2 and ABCC4 single nucleotide polymorphisms with tenofovir-associated renal toxicity.	Tenofovir	270-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
19372981-6	2008	Some other important advances in our knowledge have also been made, such as the association of TA repeats in the UGT1A1 regulatory region (UGT1A1 28) with atazanavir-related hyperbilirubinaemia and the association of ABCC2 and ABCC4 single nucleotide polymorphisms with tenofovir-associated renal toxicity.	Tenofovir	270-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
18652401-4	2008	Polymorphisms of UGT 1A1 are considered as potential indicators of a risk of toxicity treatment by irinotecan.	Irinotecan	99-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-24
18437170-4	2008	In addition, the Food and Drug Administration of the United States now requires a "black box" warning on the packaging of irinotecan for evaluation of germline polymorphism in UGT1A1, the gene mutated in Gilbert"s syndrome, for potential reduction of drug dosage in patients with the UGT1A1*28 polymorphism.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
18437170-4	2008	In addition, the Food and Drug Administration of the United States now requires a "black box" warning on the packaging of irinotecan for evaluation of germline polymorphism in UGT1A1, the gene mutated in Gilbert"s syndrome, for potential reduction of drug dosage in patients with the UGT1A1*28 polymorphism.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	284-290
18466101-1	2008	AIM: The aim of the present study was to evaluate the cost-effectiveness of UGT1A1 genotyping in second-line, high-dose, once every 3 weeks irinotecan monotherapy treatment of colorectal cancer.	Irinotecan	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
18466101-5	2008	RESULTS &amp; CONCLUSION: Genotyping in combination with a subsequent reduction of initial irinotecan dose for UGT1A1 7/7 genotype patients was cost-saving for the population of African and Caucasian origin.	Adenosine Monophosphate	9-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
18466101-5	2008	RESULTS &amp; CONCLUSION: Genotyping in combination with a subsequent reduction of initial irinotecan dose for UGT1A1 7/7 genotype patients was cost-saving for the population of African and Caucasian origin.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
18466101-8	2008	Finally, the application of a 3-weekly high-dose treatment regimen with a 20% reduced dosage compared with the low-dose weekly irinotecan regimen in patients with UGT1A1 7/7 genotype was less expensive and is more convenient for the patient.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
18379174-2	2008	Irinotecan, an anticancer drug, is one of the models for personalized medicine, and a number of clinical studies have revealed significant associations between UGT1A1(*)28 and irinotecan toxicity.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
18328680-6	2008	PB induced CYP3A4, 3A5, 2B6 and 2A6, UGT1A1 and all transporters.	Phenobarbital	0-2	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
18021224-3	2008	uridine 5"-diphosphate-glucuronosyltransferase 1A1 (UGT1A1) glucuronidates bilirubin for solubilization in the ER.	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-50
18021224-3	2008	uridine 5"-diphosphate-glucuronosyltransferase 1A1 (UGT1A1) glucuronidates bilirubin for solubilization in the ER.	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
18021224-6	2008	CONCLUSION: These results strongly suggest that bilirubin is directly delivered to UGT1A1 from ligandin for glucuronidation.	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
18248513-6	2008	Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels.	naringenin	8-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
18248513-6	2008	Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels.	Irinotecan	84-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
18098330-7	2008	It also aimed at relating glucuronidation of riluzole to differential UGT1A1*28 genotypes.	Riluzole	45-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
17713471-5	2008	The LPV/RTV treatment also inhibited the formation of SN38 glucuronide (SN38G), as shown by the 36% decrease in the SN38G/SN38 AUCs ratio (5.9+/-1.6 vs 9.2+/-2.6, P=0.002) consistent with UGT1A1 inhibition by LPV/RTV.	7-ethyl-10-hydroxycamptothecin glucuronide	54-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
17713471-5	2008	The LPV/RTV treatment also inhibited the formation of SN38 glucuronide (SN38G), as shown by the 36% decrease in the SN38G/SN38 AUCs ratio (5.9+/-1.6 vs 9.2+/-2.6, P=0.002) consistent with UGT1A1 inhibition by LPV/RTV.	Lopinavir	4-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
17713471-5	2008	The LPV/RTV treatment also inhibited the formation of SN38 glucuronide (SN38G), as shown by the 36% decrease in the SN38G/SN38 AUCs ratio (5.9+/-1.6 vs 9.2+/-2.6, P=0.002) consistent with UGT1A1 inhibition by LPV/RTV.	Ritonavir	8-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
18187562-0	2008	Contribution of UDP-glucuronosyltransferase 1A1 and 1A8 to morphine-6-glucuronidation and its kinetic properties.	Morphine	59-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-55
18187562-5	2008	Not only UGT2B7, which is well known to catalyze morphine-6-glucuronidation, but also UGT1A1 and 1A8 effectively catalyzed morphine-6-glucuronidation at relatively low morphine concentrations (&lt;100 muM).	Morphine	49-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
18187562-5	2008	Not only UGT2B7, which is well known to catalyze morphine-6-glucuronidation, but also UGT1A1 and 1A8 effectively catalyzed morphine-6-glucuronidation at relatively low morphine concentrations (&lt;100 muM).	Morphine	123-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
18187562-5	2008	Not only UGT2B7, which is well known to catalyze morphine-6-glucuronidation, but also UGT1A1 and 1A8 effectively catalyzed morphine-6-glucuronidation at relatively low morphine concentrations (&lt;100 muM).	Morphine	123-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
18187562-11	2008	The results strongly suggest that UGT1A1 and UGT1A8 are isozymes involved in morphine-6-glucuronidation in vivo, as is UGT2B7 in humans.	Morphine	77-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
18467239-0	2008	UGT1A1*28 and other UGT1A polymorphisms as determinants of irinotecan toxicity.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18379174-2	2008	Irinotecan, an anticancer drug, is one of the models for personalized medicine, and a number of clinical studies have revealed significant associations between UGT1A1(*)28 and irinotecan toxicity.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
18379174-6	2008	This mini-review outlines our recent studies on irinotecan pharmacogenetics and discusses the clinical significance of UGT1A1(*)6 and (*)28 markers for personalized irinotecan therapy in Japanese cancer patients.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
18180294-1	2008	The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin.	Bile Acids and Salts	166-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-60
18180294-1	2008	The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin.	Fatty Acids	178-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-60
18180294-1	2008	The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin.	Steroids	191-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-60
18180294-1	2008	The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin.	Bilirubin	234-243	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-60
18180294-4	2008	Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1(-/-) mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1(+/-) or wild-type mice.	Bilirubin	67-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
18180294-4	2008	Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1(-/-) mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1(+/-) or wild-type mice.	Bilirubin	157-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-107
18180294-5	2008	The result of extreme unconjugated bilirubin in Ugt1(-/-) mice, comparable to the induced levels noted in patients with Crigler-Najjar type 1 disease, is fatal in neonatal Ugt1(-/-) mice within 2 weeks following birth.	Bilirubin	35-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	172-176
18349289-7	2008	CONCLUSIONS: Irinotecan toxicity is more likely in patients with Gilbert"s syndrome carrying the UGT1A1*28 allele combined with reduced function UGT1A7 N129K/R131K and UGT1A7-57T/G SNP.	Irinotecan	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
18082937-0	2008	Importance of UDP-glucuronosyltransferase 1A1*6 for irinotecan toxicities in Japanese cancer patients.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-45
18082937-1	2008	Recent pharmacogenetic studies on irinotecan have revealed the impact of UDP glucuronosyltransferase (UGT) 1A1*28 on severe irinotecan toxicities.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-110
18082937-1	2008	Recent pharmacogenetic studies on irinotecan have revealed the impact of UDP glucuronosyltransferase (UGT) 1A1*28 on severe irinotecan toxicities.	Irinotecan	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-110
18082937-2	2008	Although the clinical role of UGT1A1*6, which is specifically detected in East Asian patients, in irinotecan toxicities is suggested, clear evidence remains limited.	Irinotecan	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
18082937-3	2008	To examine the impact of *6, the association of UGT1A1 genotypes with severe irinotecan toxicities was retrospectively investigated in Japanese cancer patients.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
18349289-1	2008	BACKGROUND: Gilbert"s syndrome is characterized by a functional promoter single nucleotide polymorphism (SNP) of the UDP-glucuronosyltransferase (UGT) 1A1 gene and represents a pharmacogenetic risk factor for irinotecan toxicity, but study data remain controversial.	Irinotecan	209-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-154
18349289-8	2008	Based on the ability of UGT1A7 to metabolize and eliminate the active irinotecan metabolite 7-ethyl-10-hydroxycamptothecin, the UGT1A1/UGT1A7 SNP combination haplotype appears to be a superior risk predictor than Gilbert"s syndrome alone.	Irinotecan	92-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
19003600-1	2008	The substrate spectrum of human UDP-glucuronosyltransferase 1A (UGT1A) proteins includes the glucuronidation of non-steroidal anti-inflammatory drugs, anticonvulsants, chemotherapeutics, steroid hormones, bile acids, and bilirubin.	Steroids	187-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-62
19255595-7	2008	Continual dietary exposure to chrysin and quercetin, found in fruits and vegetables, induces UGT1A1 and may reduce exposure to hydroxylated PCBs through increased glucuronidation.	chrysin	30-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
19255595-7	2008	Continual dietary exposure to chrysin and quercetin, found in fruits and vegetables, induces UGT1A1 and may reduce exposure to hydroxylated PCBs through increased glucuronidation.	Quercetin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	Irinotecan	0-6	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	7-ethyl-10-hydroxycamptothecin glucuronide	105-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	Irinotecan	105-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-3	2008	The toxicities of CPT-11 have been reported to correlate with the polymorphism of the number of TA repeats in UGT1A1 gene because of its gene transcriptional efficiency.	Irinotecan	18-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
17998297-3	2008	In the present study, we found that UGT1A1-catalyzed estradiol 3-O-glucuronide formation and UGT1A4-catalyzed imipramine N-glucuronide formation in human liver microsomes were prominently decreased in the presence of 1-naphthol, but those by recombinant human UGT1A1 and UGT1A4, respectively, were not.	estradiol 3-o-glucuronide	53-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
17998297-3	2008	In the present study, we found that UGT1A1-catalyzed estradiol 3-O-glucuronide formation and UGT1A4-catalyzed imipramine N-glucuronide formation in human liver microsomes were prominently decreased in the presence of 1-naphthol, but those by recombinant human UGT1A1 and UGT1A4, respectively, were not.	imipramine N-glucuronide	110-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	260-266
17998297-3	2008	In the present study, we found that UGT1A1-catalyzed estradiol 3-O-glucuronide formation and UGT1A4-catalyzed imipramine N-glucuronide formation in human liver microsomes were prominently decreased in the presence of 1-naphthol, but those by recombinant human UGT1A1 and UGT1A4, respectively, were not.	1-naphthol	217-227	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
17998297-4	2008	Interestingly, when recombinant UGT1A6 was added in the reaction mixture, these activities by recombinant UGT1A1 and UGT1A4 were diminished in the presence of 1-naphthol.	1-naphthol	159-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
17998297-6	2008	We found that UDP strongly inhibited the UGT1A1 (K(i) = 7 microM) and UGT1A4 (K(i) = 47 microM) activities in a competitive manner for the 5"-diphosphoglucuronic acid binding.	Uridine Diphosphate	14-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
17998297-6	2008	We found that UDP strongly inhibited the UGT1A1 (K(i) = 7 microM) and UGT1A4 (K(i) = 47 microM) activities in a competitive manner for the 5"-diphosphoglucuronic acid binding.	5"-diphosphoglucuronic acid	139-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
17998297-9	2008	Among them, 4 compounds (1-naphthol, 2-naphthol, 4-nitrophenol, and 4-methylumbelliferone) with high turnover rates (V(max)/K(m) value &gt;200 mul/min/mg) showed more potent inhibition of the activity in human liver microsomes compared with that by the recombinant UGT1A1.	1-naphthol	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	265-271
17998297-9	2008	Among them, 4 compounds (1-naphthol, 2-naphthol, 4-nitrophenol, and 4-methylumbelliferone) with high turnover rates (V(max)/K(m) value &gt;200 mul/min/mg) showed more potent inhibition of the activity in human liver microsomes compared with that by the recombinant UGT1A1.	2-naphthol	37-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	265-271
17998297-9	2008	Among them, 4 compounds (1-naphthol, 2-naphthol, 4-nitrophenol, and 4-methylumbelliferone) with high turnover rates (V(max)/K(m) value &gt;200 mul/min/mg) showed more potent inhibition of the activity in human liver microsomes compared with that by the recombinant UGT1A1.	4-nitrophenol	49-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	265-271
17998297-9	2008	Among them, 4 compounds (1-naphthol, 2-naphthol, 4-nitrophenol, and 4-methylumbelliferone) with high turnover rates (V(max)/K(m) value &gt;200 mul/min/mg) showed more potent inhibition of the activity in human liver microsomes compared with that by the recombinant UGT1A1.	Hymecromone	68-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	265-271
17952380-3	2008	Unconjugated bilirubin is conjugated with glucuronic acid through the reaction of uridine 5"-diphosphate-glucuronosyl transferase 1A1 (UGT1A1).	Bilirubin	13-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-133
17952380-3	2008	Unconjugated bilirubin is conjugated with glucuronic acid through the reaction of uridine 5"-diphosphate-glucuronosyl transferase 1A1 (UGT1A1).	Bilirubin	13-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
17952380-3	2008	Unconjugated bilirubin is conjugated with glucuronic acid through the reaction of uridine 5"-diphosphate-glucuronosyl transferase 1A1 (UGT1A1).	Glucuronic Acid	42-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-133
17952380-3	2008	Unconjugated bilirubin is conjugated with glucuronic acid through the reaction of uridine 5"-diphosphate-glucuronosyl transferase 1A1 (UGT1A1).	Glucuronic Acid	42-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
17952380-10	2008	Although the concentration of bilirubin in the UGT1A1 variant was higher than the wild type for the patients in the CAD group, there was no significant difference in the polymorphism of UGT1A1 between the patients in the CAD group and the participants in the control group.	Bilirubin	30-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
19003600-1	2008	The substrate spectrum of human UDP-glucuronosyltransferase 1A (UGT1A) proteins includes the glucuronidation of non-steroidal anti-inflammatory drugs, anticonvulsants, chemotherapeutics, steroid hormones, bile acids, and bilirubin.	Steroids	187-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-69
19003600-1	2008	The substrate spectrum of human UDP-glucuronosyltransferase 1A (UGT1A) proteins includes the glucuronidation of non-steroidal anti-inflammatory drugs, anticonvulsants, chemotherapeutics, steroid hormones, bile acids, and bilirubin.	Bile Acids and Salts	205-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-62
19003600-1	2008	The substrate spectrum of human UDP-glucuronosyltransferase 1A (UGT1A) proteins includes the glucuronidation of non-steroidal anti-inflammatory drugs, anticonvulsants, chemotherapeutics, steroid hormones, bile acids, and bilirubin.	Bile Acids and Salts	205-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-69
19003600-1	2008	The substrate spectrum of human UDP-glucuronosyltransferase 1A (UGT1A) proteins includes the glucuronidation of non-steroidal anti-inflammatory drugs, anticonvulsants, chemotherapeutics, steroid hormones, bile acids, and bilirubin.	Bilirubin	221-230	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-62
19003600-1	2008	The substrate spectrum of human UDP-glucuronosyltransferase 1A (UGT1A) proteins includes the glucuronidation of non-steroidal anti-inflammatory drugs, anticonvulsants, chemotherapeutics, steroid hormones, bile acids, and bilirubin.	Bilirubin	221-230	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-69
18392554-2	2008	We investigated whether the (TA)n promoter polymorphism in the UDP-glucuronosyltransferase 1A1 gene (UGT1A1) may modify bilirubin metabolism, influencing bilirubinaemia, predisposition to cholelithiasis and subsequent cholecystectomy, in a group of 153 young SCD patients (mean age 12.0 +/- 9.0 years) predominantly of Bantu beta S haplotype.	Bilirubin	120-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-94
18305373-4	2008	Rif, Dex, and Ome increased the mRNA level of UGT1A1 in both human and cynomolgus monkey hepatocytes, Ome more potently in humans and Rif and Ome more potently in monkeys.	Rifampin	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18305373-4	2008	Rif, Dex, and Ome increased the mRNA level of UGT1A1 in both human and cynomolgus monkey hepatocytes, Ome more potently in humans and Rif and Ome more potently in monkeys.	Dexamethasone	5-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18305373-4	2008	Rif, Dex, and Ome increased the mRNA level of UGT1A1 in both human and cynomolgus monkey hepatocytes, Ome more potently in humans and Rif and Ome more potently in monkeys.	Omeprazole	14-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18305373-4	2008	Rif, Dex, and Ome increased the mRNA level of UGT1A1 in both human and cynomolgus monkey hepatocytes, Ome more potently in humans and Rif and Ome more potently in monkeys.	Omeprazole	102-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18305373-4	2008	Rif, Dex, and Ome increased the mRNA level of UGT1A1 in both human and cynomolgus monkey hepatocytes, Ome more potently in humans and Rif and Ome more potently in monkeys.	Rifampin	134-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18305373-4	2008	Rif, Dex, and Ome increased the mRNA level of UGT1A1 in both human and cynomolgus monkey hepatocytes, Ome more potently in humans and Rif and Ome more potently in monkeys.	Omeprazole	102-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18095922-5	2008	Raltegravir is not a potent inhibitor or inducer of cytochrome P450 3A4, and it is predominantly metabolized by glucuronidation, specifically by the enzyme UDP-glucuronosyltransferase 1A1.	Raltegravir Potassium	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-187
18392554-2	2008	We investigated whether the (TA)n promoter polymorphism in the UDP-glucuronosyltransferase 1A1 gene (UGT1A1) may modify bilirubin metabolism, influencing bilirubinaemia, predisposition to cholelithiasis and subsequent cholecystectomy, in a group of 153 young SCD patients (mean age 12.0 +/- 9.0 years) predominantly of Bantu beta S haplotype.	Bilirubin	120-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
18098064-0	2008	Regulation of UDP-glucuronosyltransferase (UGT) 1A1 by progesterone and its impact on labetalol elimination.	Progesterone	55-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-51
17921187-4	2008	HLMs, UGT1A1, 1A8, 1A9, and 1A10 showed glucuronidation activity toward 4"-, 6-, 7-, and/or 8-hydroxywarfarin with K(m) values ranging from 59 to 480 microM and V(max) values ranging from 0.03 to 0.78 microM/min/mg protein.	4"-, 6-, 7-, and/	72-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
17921187-4	2008	HLMs, UGT1A1, 1A8, 1A9, and 1A10 showed glucuronidation activity toward 4"-, 6-, 7-, and/or 8-hydroxywarfarin with K(m) values ranging from 59 to 480 microM and V(max) values ranging from 0.03 to 0.78 microM/min/mg protein.	8-hydroxywarfarin	92-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
17921187-6	2008	Of the hepatic UGT isozymes tested, UGT1A9 exclusively metabolized 8-hydroxywarfarin, whereas UGT1A1 metabolized 6-, 7-, and 8-hydroxywarfarin.	6-, 7-, and 8-hydroxywarfarin	113-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
18043502-3	2008	(TA)7 promoter polymorphism in the gene encoding the bilirubin conjugating enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1) potentiates hyperbilirubinemia in G-6-PD deficient neonates.	Bilirubin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-113
18043502-3	2008	(TA)7 promoter polymorphism in the gene encoding the bilirubin conjugating enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1) potentiates hyperbilirubinemia in G-6-PD deficient neonates.	Bilirubin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
18098064-0	2008	Regulation of UDP-glucuronosyltransferase (UGT) 1A1 by progesterone and its impact on labetalol elimination.	Labetalol	86-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-51
18098064-3	2008	Labetalol glucuronidation, which is the major elimination pathway of labetalol, was characterized by screening six recombinant human UGTs (UGT1A1, 1A4, 1A6, 1A9, 2B4, and 2B7) for their capacity to catalyse labetalol glucuronidation.	Labetalol	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
18098064-6	2008	UGT1A1 and UGT2B7 were identified as the major UGT enzymes producing labetalol glucuronides (trace amount of glucuronide conjugate was formed by UGT1A9).	labetalol glucuronides	69-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18098064-6	2008	UGT1A1 and UGT2B7 were identified as the major UGT enzymes producing labetalol glucuronides (trace amount of glucuronide conjugate was formed by UGT1A9).	Glucuronides	79-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18098064-7	2008	The activities of the UGT1A1 promoter containing PXR response elements were enhanced by progesterone, but not by oestrogens, indicating PXR-mediated induction of UGT1A1 promoter activity by progesterone.	Progesterone	88-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
18098064-7	2008	The activities of the UGT1A1 promoter containing PXR response elements were enhanced by progesterone, but not by oestrogens, indicating PXR-mediated induction of UGT1A1 promoter activity by progesterone.	Progesterone	88-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
18098064-7	2008	The activities of the UGT1A1 promoter containing PXR response elements were enhanced by progesterone, but not by oestrogens, indicating PXR-mediated induction of UGT1A1 promoter activity by progesterone.	Progesterone	190-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
18098064-7	2008	The activities of the UGT1A1 promoter containing PXR response elements were enhanced by progesterone, but not by oestrogens, indicating PXR-mediated induction of UGT1A1 promoter activity by progesterone.	Progesterone	190-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
18098064-11	2008	The results suggest a potential role for progesterone in regulating labetalol elimination by modulating the expression of UGT1A1, leading to enhanced drug metabolism during pregnancy.	Labetalol	68-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
17761779-7	2007	Mefenamic acid, a UGT1A9 inhibitor, decreased FYX-051 N(1)- and N(2)-glucuronosyltransferase activities, whereas bilirubin, a UGT1A1 inhibitor, did not affect these activities.	Bilirubin	113-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
17956868-10	2007	Furthermore, mutation of His-39 residue of UGT1A1 (His-40 in UGT1A4) to proline led to loss of glucuronidation of phenols but not of estrogens.	Histidine	25-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17956868-10	2007	Furthermore, mutation of His-39 residue of UGT1A1 (His-40 in UGT1A4) to proline led to loss of glucuronidation of phenols but not of estrogens.	Histidine	51-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17956868-10	2007	Furthermore, mutation of His-39 residue of UGT1A1 (His-40 in UGT1A4) to proline led to loss of glucuronidation of phenols but not of estrogens.	Proline	72-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17956868-10	2007	Furthermore, mutation of His-39 residue of UGT1A1 (His-40 in UGT1A4) to proline led to loss of glucuronidation of phenols but not of estrogens.	Phenols	114-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17981384-6	2007	Compared with control cells (MCF-7(VEC)), reduced cell proliferation was seen in cells expressing UGT1A1 (MCF-7(UGT1A1)) under estradiol treatment.	Estradiol	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
17981384-6	2007	Compared with control cells (MCF-7(VEC)), reduced cell proliferation was seen in cells expressing UGT1A1 (MCF-7(UGT1A1)) under estradiol treatment.	Estradiol	127-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
17981384-8	2007	Over-expressing UGT1A1 reduced the binding of DMBA to DNA, and increased MCF-7(UGT1A1) intact cells under DMBA treatment was verified by comet assay.	9,10-Dimethyl-1,2-benzanthracene	46-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
17981384-8	2007	Over-expressing UGT1A1 reduced the binding of DMBA to DNA, and increased MCF-7(UGT1A1) intact cells under DMBA treatment was verified by comet assay.	9,10-Dimethyl-1,2-benzanthracene	106-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
17981384-8	2007	Over-expressing UGT1A1 reduced the binding of DMBA to DNA, and increased MCF-7(UGT1A1) intact cells under DMBA treatment was verified by comet assay.	9,10-Dimethyl-1,2-benzanthracene	106-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
17875670-5	2007	All the UGTs examined catalyzed the formation of T4 phenolic glucuronide except UGT1A4; the highest activity was detected with UGT1A3, UGT1A8, and UGT1A10, followed by UGT1A1 and UGT2B4.	Glucuronides	61-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
18004206-2	2007	This work compared the effects of (a) the individual UGT1A1 mutations on the glucuronidation kinetics bilirubin, beta-estradiol, 4-methylumbelliferone (4MU) and 1-naphthol (1NP), and (b) the Y486 mutation, which occurs in the conserved carboxyl terminal domain of UGT1A enzymes, on 4MU, 1NP and naproxen glucuronidation by UGT1A3, UGT1A6 and UGT1A10.	Bilirubin	102-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
17875670-6	2007	Formation of T3 phenolic glucuronide was observed in the order of UGT1A8 &gt; UGT1A10 &gt; UGT1A3 &gt; UGT1A1; trace activity was observed with UGT1A6 and UGT1A9.	t3 phenolic glucuronide	13-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
17898154-1	2007	The UGT1A1*28 polymorphism is known to correlate with altered clearance of bilirubin (Gilbert syndrome) and drugs such as 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11).	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
17898154-1	2007	The UGT1A1*28 polymorphism is known to correlate with altered clearance of bilirubin (Gilbert syndrome) and drugs such as 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11).	Irinotecan	122-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
17898154-1	2007	The UGT1A1*28 polymorphism is known to correlate with altered clearance of bilirubin (Gilbert syndrome) and drugs such as 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11).	Irinotecan	191-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
17898154-5	2007	Bilirubin, estradiol (3-OH), ethinyl estradiol (3-OH), and 7-ethyl-10-hydroxycamptothecin (SN-38) were found to show significantly lower rates of metabolism in the UGT1A1*28/*28 microsomes with no change in K(m) values.	Irinotecan	59-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
17898154-8	2007	Interestingly, muraglitazar (UGT1A3 substrate) showed an inverse correlation with glucuronidation of UGT1A1 substrates.	muraglitazar	15-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
18004206-2	2007	This work compared the effects of (a) the individual UGT1A1 mutations on the glucuronidation kinetics bilirubin, beta-estradiol, 4-methylumbelliferone (4MU) and 1-naphthol (1NP), and (b) the Y486 mutation, which occurs in the conserved carboxyl terminal domain of UGT1A enzymes, on 4MU, 1NP and naproxen glucuronidation by UGT1A3, UGT1A6 and UGT1A10.	Estradiol	113-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
18004206-2	2007	This work compared the effects of (a) the individual UGT1A1 mutations on the glucuronidation kinetics bilirubin, beta-estradiol, 4-methylumbelliferone (4MU) and 1-naphthol (1NP), and (b) the Y486 mutation, which occurs in the conserved carboxyl terminal domain of UGT1A enzymes, on 4MU, 1NP and naproxen glucuronidation by UGT1A3, UGT1A6 and UGT1A10.	Hymecromone	129-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
18004206-5	2007	RESULTS: Compared with wild-type UGT1A1, in-vitro clearances for bilirubin, beta-estradiol, 4MU and 1NP glucuronidation by UGT1A1*6 and UGT1A1*27 were reduced by 34-74%, most commonly as a result of a reduction in Vmax.	Bilirubin	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
18004206-5	2007	RESULTS: Compared with wild-type UGT1A1, in-vitro clearances for bilirubin, beta-estradiol, 4MU and 1NP glucuronidation by UGT1A1*6 and UGT1A1*27 were reduced by 34-74%, most commonly as a result of a reduction in Vmax.	Bilirubin	65-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
18004206-5	2007	RESULTS: Compared with wild-type UGT1A1, in-vitro clearances for bilirubin, beta-estradiol, 4MU and 1NP glucuronidation by UGT1A1*6 and UGT1A1*27 were reduced by 34-74%, most commonly as a result of a reduction in Vmax.	Estradiol	76-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
18004206-5	2007	RESULTS: Compared with wild-type UGT1A1, in-vitro clearances for bilirubin, beta-estradiol, 4MU and 1NP glucuronidation by UGT1A1*6 and UGT1A1*27 were reduced by 34-74%, most commonly as a result of a reduction in Vmax.	Estradiol	76-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
17927138-5	2007	The results also indicated that well-expressed UGT isoforms in the Caco-2 cells, UGT1A1, UGT1A3, UGT1A6, and UGT2B7, were capable of metabolizing apigenin faster than genistein and that UGT1A6 silencing did not substantially increase the level of expression of genistein-metabolizing UGT isoforms.	Apigenin	146-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
17978490-0	2007	Stereoselective metabolism of racemic carvedilol by UGT1A1 and UGT2B7, and effects of mutation of these enzymes on glucuronidation activity.	Carvedilol	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
17978490-1	2007	Carvedilol, an alpha- and beta-adrenergic blocking drug, is mainly metabolized by CYP2D6, UGT1A1, UGT2B4 and UGT2B7.	Carvedilol	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
17978490-6	2007	The aim of this study was to clarify stereoselective metabolism of carvedilol by UGT1A1 and UGT2B7 and to determine by using a recombinant enzyme-introduced mutation whether genetic mutation in UGT1A1 and UGT2B7 causes reduction in metabolic activity for carvedilol.	Carvedilol	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
17978490-6	2007	The aim of this study was to clarify stereoselective metabolism of carvedilol by UGT1A1 and UGT2B7 and to determine by using a recombinant enzyme-introduced mutation whether genetic mutation in UGT1A1 and UGT2B7 causes reduction in metabolic activity for carvedilol.	Carvedilol	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
17978490-6	2007	The aim of this study was to clarify stereoselective metabolism of carvedilol by UGT1A1 and UGT2B7 and to determine by using a recombinant enzyme-introduced mutation whether genetic mutation in UGT1A1 and UGT2B7 causes reduction in metabolic activity for carvedilol.	Carvedilol	255-265	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
17978490-7	2007	A glucuronidation assay using human liver microsomes and recombinant UGT1A1 and UGT2B7 expressed in HeLa cells demonstrated that UGT1A1 prefers metabolizing R-carvedilol to S-carvedilol.	Carvedilol	157-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
17978490-7	2007	A glucuronidation assay using human liver microsomes and recombinant UGT1A1 and UGT2B7 expressed in HeLa cells demonstrated that UGT1A1 prefers metabolizing R-carvedilol to S-carvedilol.	Carvedilol	157-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
17978490-7	2007	A glucuronidation assay using human liver microsomes and recombinant UGT1A1 and UGT2B7 expressed in HeLa cells demonstrated that UGT1A1 prefers metabolizing R-carvedilol to S-carvedilol.	Carvedilol	173-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
17611564-5	2007	As nilotinib is not known to be glucuronidated by UGT1A1, the combined impact of inhibition of UGT1A1 activity by nilotinib and genetic polymorphism is the most likely cause of the increased rate of hyperbilirubinemia.	nilotinib	3-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
17611564-5	2007	As nilotinib is not known to be glucuronidated by UGT1A1, the combined impact of inhibition of UGT1A1 activity by nilotinib and genetic polymorphism is the most likely cause of the increased rate of hyperbilirubinemia.	nilotinib	114-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
17888052-1	2007	AIM: To investigate bilirubin UDP-glucuronosyltransferase (UGT1A1) gene allele in healthy Chinese neonates, their cord bilirubin level and the subsequent hyperbilirubinemia to determine relationships among them.	Bilirubin	20-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
17888052-1	2007	AIM: To investigate bilirubin UDP-glucuronosyltransferase (UGT1A1) gene allele in healthy Chinese neonates, their cord bilirubin level and the subsequent hyperbilirubinemia to determine relationships among them.	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
17611564-0	2007	UGT1A1 promoter polymorphism increases risk of nilotinib-induced hyperbilirubinemia.	nilotinib	47-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17611564-3	2007	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) glucuronidates bilirubin in humans, and a polymorphism in the promoter of the gene that encodes it has been associated with hyperbilirubinemia during treatment with a number of drugs.	Bilirubin	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-47
17611564-3	2007	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) glucuronidates bilirubin in humans, and a polymorphism in the promoter of the gene that encodes it has been associated with hyperbilirubinemia during treatment with a number of drugs.	Bilirubin	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
17927138-5	2007	The results also indicated that well-expressed UGT isoforms in the Caco-2 cells, UGT1A1, UGT1A3, UGT1A6, and UGT2B7, were capable of metabolizing apigenin faster than genistein and that UGT1A6 silencing did not substantially increase the level of expression of genistein-metabolizing UGT isoforms.	Genistein	167-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
17927138-5	2007	The results also indicated that well-expressed UGT isoforms in the Caco-2 cells, UGT1A1, UGT1A3, UGT1A6, and UGT2B7, were capable of metabolizing apigenin faster than genistein and that UGT1A6 silencing did not substantially increase the level of expression of genistein-metabolizing UGT isoforms.	Genistein	261-270	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
29793274-7	2007	In that study, a statistically significantly higher level of SN-38 and a relatively lower degree of glucuronidation occurred in patients with the UGT1A1*6 homozygote genotype than in patients with the reference genotype.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
17060921-1	2007	Variants within the human UGT1A1 gene are associated with irinotecan induced severely adverse reactions and hyperbilirubinemia.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
17620344-6	2007	The coexpression of both UGT1A1 and UGT1A4 increased the V(max) values of UGT1A6-catalyzed serotonin and diclofenac O-glucuronide formation.	Serotonin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
17620344-6	2007	The coexpression of both UGT1A1 and UGT1A4 increased the V(max) values of UGT1A6-catalyzed serotonin and diclofenac O-glucuronide formation.	1-O-(2-((2',6'-dichlorophenyl)amino)phenylacetyl)glucopyranuronic acid	105-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
17620344-2	2007	The substrates specific for UGT1A1 (estradiol and bilirubin), UGT1A4 (imipramine and trifluoperazine), and UGT1A6 (serotonin and diclofenac) were used to determine the effects of the coexpression of the other UGT1A isoforms on the enzymatic activity.	Trifluoperazine	85-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
17620344-3	2007	The coexpression of UGT1A4 and UGT1A6 decreased the S(50) and V(max) values of UGT1A1-catalyzed estradiol 3-O-glucuronide formation and increased the V(max) value of UGT1A1-catalyzed bilirubin O-glucuronide formation.	estradiol 3-o-glucuronide	96-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
17620344-3	2007	The coexpression of UGT1A4 and UGT1A6 decreased the S(50) and V(max) values of UGT1A1-catalyzed estradiol 3-O-glucuronide formation and increased the V(max) value of UGT1A1-catalyzed bilirubin O-glucuronide formation.	Bilirubin	183-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
17620344-3	2007	The coexpression of UGT1A4 and UGT1A6 decreased the S(50) and V(max) values of UGT1A1-catalyzed estradiol 3-O-glucuronide formation and increased the V(max) value of UGT1A1-catalyzed bilirubin O-glucuronide formation.	o-glucuronide	108-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
17620344-4	2007	The coexpression of UGT1A1 decreased the V(max) value of UGT1A4-catalyzed imipramine N-glucuronide formation but had no effect on UGT1A4-catalyzed trifluoperazine N-glucuronide formation.	imipramine N-glucuronide	74-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
17060921-3	2007	Relationship between the concentrations of total serum bilirubin (T-bil) and haplotype structure of UGT1A1 in healthy people were also evaluated.	Bilirubin	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
17060921-3	2007	Relationship between the concentrations of total serum bilirubin (T-bil) and haplotype structure of UGT1A1 in healthy people were also evaluated.	bil	55-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
17728214-1	2007	The Food and Drug Administration and Pfizer changed the package insert for irinotecan to include a patient"s UGT1A1*28 genotype as a risk factor for severe neutropenia on the basis of the findings of four pharmacogenetic studies, which found that irinotecan-treated patients who were homozygous for the UGT1A1*28 allele had a greater risk of hematologic toxic effects than patients who had one or two copies of the wild-type allele (UGT1A1*1).	Irinotecan	75-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17898662-2	2007	Polymorphism of the UGT1A1 gene is one of the likely reasons for interindividual differences in irinotecan pharmacokinetics and severe toxicity.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	297-302	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
17728214-7	2007	The risk of experiencing irinotecan-induced hematologic toxicity for patients with a UGT1A1*28/*28 genotype thus appears to be a function of the dose of irinotecan administered.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
17728214-1	2007	The Food and Drug Administration and Pfizer changed the package insert for irinotecan to include a patient"s UGT1A1*28 genotype as a risk factor for severe neutropenia on the basis of the findings of four pharmacogenetic studies, which found that irinotecan-treated patients who were homozygous for the UGT1A1*28 allele had a greater risk of hematologic toxic effects than patients who had one or two copies of the wild-type allele (UGT1A1*1).	Irinotecan	247-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17728214-7	2007	The risk of experiencing irinotecan-induced hematologic toxicity for patients with a UGT1A1*28/*28 genotype thus appears to be a function of the dose of irinotecan administered.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
17697043-0	2007	Substrate-dependent modulation of UDP-glucuronosyltransferase 1A1 (UGT1A1) by propofol in recombinant human UGT1A1 and human liver microsomes.	Propofol	78-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-65
17697043-0	2007	Substrate-dependent modulation of UDP-glucuronosyltransferase 1A1 (UGT1A1) by propofol in recombinant human UGT1A1 and human liver microsomes.	Propofol	78-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
17697043-0	2007	Substrate-dependent modulation of UDP-glucuronosyltransferase 1A1 (UGT1A1) by propofol in recombinant human UGT1A1 and human liver microsomes.	Propofol	78-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
17697043-1	2007	Our previous study has shown that propofol, a probe substrate for human UDP-glucuronosyltransferase (UGT) 1A9, activated the glucuronidation of 4-methylumbelliferone (4-MU) by recombinant UGT1A1 in a concentration-dependent manner.	Propofol	34-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
17697043-1	2007	Our previous study has shown that propofol, a probe substrate for human UDP-glucuronosyltransferase (UGT) 1A9, activated the glucuronidation of 4-methylumbelliferone (4-MU) by recombinant UGT1A1 in a concentration-dependent manner.	Hymecromone	144-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
17697043-6	2007	In contrast to 4-MUG activity, propofol inhibited UGT1A1-catalysed oestradiol 3beta-glucuronidation in recombinant UGT1A1 as well as in human liver microsomes with IC(50) values of 59 and 228 microM, respectively.	Propofol	31-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
17697043-6	2007	In contrast to 4-MUG activity, propofol inhibited UGT1A1-catalysed oestradiol 3beta-glucuronidation in recombinant UGT1A1 as well as in human liver microsomes with IC(50) values of 59 and 228 microM, respectively.	Propofol	31-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
17697043-6	2007	In contrast to 4-MUG activity, propofol inhibited UGT1A1-catalysed oestradiol 3beta-glucuronidation in recombinant UGT1A1 as well as in human liver microsomes with IC(50) values of 59 and 228 microM, respectively.	Estradiol	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
17697043-6	2007	In contrast to 4-MUG activity, propofol inhibited UGT1A1-catalysed oestradiol 3beta-glucuronidation in recombinant UGT1A1 as well as in human liver microsomes with IC(50) values of 59 and 228 microM, respectively.	Estradiol	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
17697043-7	2007	In addition, a known UGT1A1 modulator, 17alpha-ethynyloestradiol, stimulated oestradiol 3beta-glucuronidation slightly at a concentration of 5 microM, while it inhibited 4-MUG in recombinant UGT1A1 at all concentrations tested (5-100 microM).	Ethinyl Estradiol	39-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
17697043-7	2007	In addition, a known UGT1A1 modulator, 17alpha-ethynyloestradiol, stimulated oestradiol 3beta-glucuronidation slightly at a concentration of 5 microM, while it inhibited 4-MUG in recombinant UGT1A1 at all concentrations tested (5-100 microM).	Ethinyl Estradiol	39-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
17697043-7	2007	In addition, a known UGT1A1 modulator, 17alpha-ethynyloestradiol, stimulated oestradiol 3beta-glucuronidation slightly at a concentration of 5 microM, while it inhibited 4-MUG in recombinant UGT1A1 at all concentrations tested (5-100 microM).	Estradiol	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
17697043-7	2007	In addition, a known UGT1A1 modulator, 17alpha-ethynyloestradiol, stimulated oestradiol 3beta-glucuronidation slightly at a concentration of 5 microM, while it inhibited 4-MUG in recombinant UGT1A1 at all concentrations tested (5-100 microM).	Estradiol	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
17697043-8	2007	These findings indicate that the modulation of UGT1A1 by propofol is substrate-dependent, and thus care should be taken when extrapolating the stimulatory effects of drugs for one glucuronidation substrate.	Propofol	57-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
17627617-7	2007	These exploratory findings suggest that homozygosity for UGT1A1*6 allele may be associated with altered SN-38 disposition and may increase the risk of severe neutropenia in Asian cancer patients, particularly in the Chinese cancer patients who comprised 80% (n = 36) of the patient population in the present study.	Irinotecan	104-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
17406868-0	2007	Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6 is associated with reduced activity for SN-38 in Japanese patients with cancer.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
17406868-9	2007	CONCLUSION: Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6, related to reduced catalytic and transcriptional activities of UGTs, is associated with the decreased glucuronosyltransferase activity for SN-38 in Japanese patients with cancer.	Irinotecan	215-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
17591678-9	2007	Collectively, the data indicate that the major mechanism of clearance of raltegravir in humans is UGT1A1-mediated glucuronidation.	Raltegravir Potassium	73-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
17591679-8	2007	Kinetic and inhibition analyses suggested that the thyroxine glucuronidation in human jejunum microsomes was mainly catalyzed by UGT1A8 and UGT1A10 and to a lesser extent by UGT1A1, and the activity in human kidney microsomes was mainly catalyzed by UGT1A7, UGT1A9, and UGT1A10.	Thyroxine	51-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
17576806-0	2007	Stereoselective glucuronidation of 5-(4"-hydroxyphenyl)-5-phenylhydantoin by human UDP-glucuronosyltransferase (UGT) 1A1, UGT1A9, and UGT2B15: effects of UGT-UGT interactions.	hydroxyphenytoin	35-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-120
17576806-6	2007	Among human UDP-glucuronosyltransferase (UGT) enzymes, UGT1A1, UGT1A9, and UGT2B15 showed 4"-HPPH O-glucuronide formation.	o-glucuronide	98-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
17478602-9	2007	The correlation of UGT1A1 with total bilirubin levels was mainly due to (TA)(n) repeats in Caucasians but a clear correlation was not observed in African Americans because of the high diversity of haplotypes and the small sample size.	Bilirubin	37-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
17576806-7	2007	Interestingly, UGT1A1 stereoselectively formed (R)-4"-HPPH O-glucuronide, whereas UGT1A9 and UGT2B15 stereoselectively formed (S)-4"-HPPH O-glucuronide from racemic 4"-HPPH.	(r)-4"-hpph o-glucuronide	47-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17576806-7	2007	Interestingly, UGT1A1 stereoselectively formed (R)-4"-HPPH O-glucuronide, whereas UGT1A9 and UGT2B15 stereoselectively formed (S)-4"-HPPH O-glucuronide from racemic 4"-HPPH.	hydroxyphenytoin	51-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17576806-9	2007	It was demonstrated that coexpression of UGT1A4 increased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A1 but decreased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A9.	Sulfur	79-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
17576806-9	2007	It was demonstrated that coexpression of UGT1A4 increased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A1 but decreased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A9.	(r)-4"-hpph o-glucuronide	88-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
17576806-9	2007	It was demonstrated that coexpression of UGT1A4 increased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A1 but decreased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A9.	Sulfur	179-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
17576806-9	2007	It was demonstrated that coexpression of UGT1A4 increased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A1 but decreased the V(max) values of (S)- and (R)-4"-HPPH O-glucuronide formation catalyzed by UGT1A9.	(r)-4"-hpph o-glucuronide	188-213	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
17576806-10	2007	Coexpression of UGT1A6 increased the S(50) values and decreased the V(max) values of (S)- and (R)-4"-HPPH glucuronide formation catalyzed by UGT1A1 and UGT1A9.	3-azido-2,7-naphthalene disulfonate	85-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
17576806-10	2007	Coexpression of UGT1A6 increased the S(50) values and decreased the V(max) values of (S)- and (R)-4"-HPPH glucuronide formation catalyzed by UGT1A1 and UGT1A9.	(r)-4"-hpph glucuronide	94-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
17576806-12	2007	In conclusion, we found that 4"-HPPH O-glucuronide formation in human liver microsomes is catalyzed by UGT1A1, UGT1A9, and UGT2B15 in a stereoselective manner, being modulated by interaction with other UGT1A isoforms.	4"-hpph o-glucuronide	29-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
17691917-5	2007	So far, the candidate gene approach has provided important clues for pharmacogenomic-based personalized chemotherapy with 6-mercaptopurine (6-MP), solely metabolized by thiopurine S-methyltransferase (TPMT), and irinotecan, mainly detoxified by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Mercaptopurine	122-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	245-276
17691917-5	2007	So far, the candidate gene approach has provided important clues for pharmacogenomic-based personalized chemotherapy with 6-mercaptopurine (6-MP), solely metabolized by thiopurine S-methyltransferase (TPMT), and irinotecan, mainly detoxified by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Mercaptopurine	122-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	278-284
17691917-5	2007	So far, the candidate gene approach has provided important clues for pharmacogenomic-based personalized chemotherapy with 6-mercaptopurine (6-MP), solely metabolized by thiopurine S-methyltransferase (TPMT), and irinotecan, mainly detoxified by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Mercaptopurine	140-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	245-276
17691917-5	2007	So far, the candidate gene approach has provided important clues for pharmacogenomic-based personalized chemotherapy with 6-mercaptopurine (6-MP), solely metabolized by thiopurine S-methyltransferase (TPMT), and irinotecan, mainly detoxified by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Mercaptopurine	140-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	278-284
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Mercaptopurine	158-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Mercaptopurine	158-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17628876-4	2007	The phenolic glucuronidation of the curcuminoids was predominantly catalyzed by hepatic UGT1A1 and intestinal UGT1A8 and 1A10, whereas UGT1A9, 2B7, and 1A8 exhibited high activities for hexahydro-curcuminoids.	curcuminoids	36-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
17622938-0	2007	UGT1A1*28 genotype affects the in-vitro glucuronidation of thyroxine in human livers.	Thyroxine	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17622938-6	2007	RESULTS: A strong correlation was observed between the glucuronidation of T4 and SN-38, a UGT1A1 substrate (r=0.82, P&lt;0.0001).	Irinotecan	81-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
17622938-7	2007	A significant trend of decreasing T4 glucuronide (T4G) levels was observed with increasing number of UGT1A1 -53(TA)7 alleles (P=0.001).	t4 glucuronide	34-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
17593033-5	2007	Regression analysis showed that serum bilirubin levels and the incidence of gallstones were strongly associated with the number of UGT1A1 [TA] repeats in all subjects (P &lt; 0.0001 and P &lt; 0.01, respectively).	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
17498780-7	2007	These results showed that AhR, UGT1A1, GSTP1 and GSTT1 polymorphisms were associated with urinary 1-OHP concentrations in Chinese coke oven workers.	Oxaliplatin	98-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
17762398-2	2007	The presence of an additional TA repeat in the TATA sequence of the UGT1A1 promoter leads to a significant decrease in SN-38 glucuronidation.	Irinotecan	119-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
17762398-3	2007	Patients with the UGT1A1 (TA)7 allele are more likely to experience severe neutropenia and diarrhea following irinotecan chemotherapy.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
17593033-1	2007	Serum bilirubin levels and predisposition to gallstones in sickle cell disease (SCD) are influenced by genetic variation in the hepatic uridine diphosphate (UDP)-glucuronosyltransferase (UGT1A1) gene, but the association is not consistent.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17558305-10	2007	CONCLUSIONS: The haplotypes significantly associated with reduced area under concentration curve ratios and neutropenia contained UGT1A1*6 or *28, and both of them should be genotyped before irinotecan is given to Japanese and probably other Asian patients.	Irinotecan	191-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
17593033-1	2007	Serum bilirubin levels and predisposition to gallstones in sickle cell disease (SCD) are influenced by genetic variation in the hepatic uridine diphosphate (UDP)-glucuronosyltransferase (UGT1A1) gene, but the association is not consistent.	hepatic uridine diphosphate	128-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17593033-1	2007	Serum bilirubin levels and predisposition to gallstones in sickle cell disease (SCD) are influenced by genetic variation in the hepatic uridine diphosphate (UDP)-glucuronosyltransferase (UGT1A1) gene, but the association is not consistent.	Uridine Diphosphate	157-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17681105-1	2007	BACKGROUND: Uridine diphosphate glucuronosyltransferase (UGT) 1A1 7/7 polymorphism has been linked with an increased risk of irinotecan-induced severe toxicities.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-65
17681105-2	2007	We evaluated UGT1A1 polymorphism in patients developing grade 3/4 toxicity after initiation of irinotecan to determine the frequency of this polymorphism in this population.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
17681105-3	2007	PATIENTS AND METHODS: Twenty patients with grade 3/4 irinotecan-induced toxicity underwent UGT1A1 genotyping in an exploratory study.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
17681105-8	2007	Our data support the need for more prospective studies that evaluate the predictive value of UGT1A1 as well as UGT1A1-based dosing in patients receiving irinotecan.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
17681105-8	2007	Our data support the need for more prospective studies that evaluate the predictive value of UGT1A1 as well as UGT1A1-based dosing in patients receiving irinotecan.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Bilirubin	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Bilirubin	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Phenobarbital	126-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Phenobarbital	126-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
17446261-4	2007	UGT1A1, 1A3, 1A9, 2B4, and 2B7 showed glucuronidation activity for both (R)- and (S)-glucuronide, with UGT2B7 possessing the highest activity.	(r)- and (s)-glucuronide	72-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	Pyranocoumarins	63-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	Pyranocoumarins	63-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	351-357
17426648-1	2007	Increased heme catabolism has been reported in glucose-6-phosphate dehydrogenase (G-6-PD)-normal neonates who were also homozygous for (TA)7/(TA)7 (UGT1A1*28) uridine diphosphoglucuronate-glucuronosyltransferase 1A1 (UGT) promoter polymorphism (Gilbert syndrome).	Heme	10-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	CHEMBL2334004	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	cis-avicennol	93-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	cis-avicennol	93-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	351-357
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	Furocoumarins	116-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	Furocoumarins	116-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	351-357
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	Coumarins	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	Coumarins	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	351-357
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	coumarin	69-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
17599282-5	2007	After 3 days of treatment at a concentration of 25 microM, the pyranocoumarins avicennin and CIS-avicennol, and the furocoumarins bergapten and imperatorin, increased by 2-fold UGT1A1-dependent activity, equivalent to the increases obtained with chrysin at 25 microM, whereas in the presence of the simple coumarins such as coumarin or umbelliferone, UGT1A1-dependent activity was not modified.	coumarin	69-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	351-357
17599282-6	2007	In terms of structural requirements for UGT1A1 induction, the present study suggests that the B-ring (phenyl) for chrysin and the furan or pyran rings for coumarins are essential for the biological activity.	furan	130-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
17599282-6	2007	In terms of structural requirements for UGT1A1 induction, the present study suggests that the B-ring (phenyl) for chrysin and the furan or pyran rings for coumarins are essential for the biological activity.	Pyrans	139-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
17599282-6	2007	In terms of structural requirements for UGT1A1 induction, the present study suggests that the B-ring (phenyl) for chrysin and the furan or pyran rings for coumarins are essential for the biological activity.	Coumarins	155-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
17577039-0	2007	UGT1A1 promoter genotype correlates with SN-38 pharmacokinetics, but not severe toxicity in patients receiving low-dose irinotecan.	Irinotecan	41-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17608024-0	2007	UGT1AI*6 and UGT1A1*27 for individualized irinotecan chemotherapy.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
17608024-1	2007	Genetic polymorphisms of uridine 5"-diphospho-glucuronosyl-transferase (UGT)1A1, a crucial drug-metabolizing enzyme of the anticancer drug irinotecan, are essential determinants of individual variation in susceptibility to irinotecan-related toxicity.	Uridine	25-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-79
17608024-1	2007	Genetic polymorphisms of uridine 5"-diphospho-glucuronosyl-transferase (UGT)1A1, a crucial drug-metabolizing enzyme of the anticancer drug irinotecan, are essential determinants of individual variation in susceptibility to irinotecan-related toxicity.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-79
17608024-1	2007	Genetic polymorphisms of uridine 5"-diphospho-glucuronosyl-transferase (UGT)1A1, a crucial drug-metabolizing enzyme of the anticancer drug irinotecan, are essential determinants of individual variation in susceptibility to irinotecan-related toxicity.	Irinotecan	223-233	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-79
17608024-4	2007	Therefore, it is reasonable to assume that the presence of UGT1A1*6 or UGTIA1*27 would also increase the risk of irinotecan toxicity.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
17510208-0	2007	UGT1A1 polymorphism can predict hematologic toxicity in patients treated with irinotecan.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17475008-8	2007	Molecular docking experiments identified key residues in donor and acceptor recognition and provided insight into the catalytic mechanism of UGT glucuronidation, suggesting the human UGT1A1 residue histidine 39 (H39) as a general base and the residue aspartic acid 151 (D151) as an important electron-transfer helper.	Histidine	198-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-189
17529881-4	2007	SN-38 is further metabolized to SN-38G by various hepatic and extrahepatic UGT1A isozymes, mainly UGT1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
17529881-4	2007	SN-38 is further metabolized to SN-38G by various hepatic and extrahepatic UGT1A isozymes, mainly UGT1A1.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
17529881-5	2007	Impaired glucuronidation activity of the UGT1A1 enzyme has been linked with elevated levels of SN-38, leading to toxicities.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
17529881-6	2007	UGT1A1*28 involves an extra TA repeat in the UGT1A1 promoter region and is the variant most frequently contributing to interpatient variability in irinotecan pharmacokinetics and toxicities.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17529881-6	2007	UGT1A1*28 involves an extra TA repeat in the UGT1A1 promoter region and is the variant most frequently contributing to interpatient variability in irinotecan pharmacokinetics and toxicities.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
17529881-8	2007	Recently, UGT1A1*6 seems to contribute to the risk of toxicity of irinotecan in Asian patients.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
17293379-6	2007	Using the single expression systems, it was confirmed that estradiol 3-O-glucuronide, imipramine N-glucuronide, serotonin O-glucuronide, and propofol O-glucuronide formations are specific for UGT1A1, UGT1A4, UGT1A6, and UGT1A9, respectively.	estradiol 3-o-glucuronide	59-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
17293379-6	2007	Using the single expression systems, it was confirmed that estradiol 3-O-glucuronide, imipramine N-glucuronide, serotonin O-glucuronide, and propofol O-glucuronide formations are specific for UGT1A1, UGT1A4, UGT1A6, and UGT1A9, respectively.	imipramine N-glucuronide	86-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
17293379-6	2007	Using the single expression systems, it was confirmed that estradiol 3-O-glucuronide, imipramine N-glucuronide, serotonin O-glucuronide, and propofol O-glucuronide formations are specific for UGT1A1, UGT1A4, UGT1A6, and UGT1A9, respectively.	serotonin o-glucuronide	112-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
17293379-6	2007	Using the single expression systems, it was confirmed that estradiol 3-O-glucuronide, imipramine N-glucuronide, serotonin O-glucuronide, and propofol O-glucuronide formations are specific for UGT1A1, UGT1A4, UGT1A6, and UGT1A9, respectively.	propofol o-glucuronide	141-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
17293379-8	2007	On the other hand, the coexpressed UGT1A1 increased Km and decreased the Vmax of the propofol O-glucuronide formation catalyzed by UGT1A9.	Propofol	85-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
17293379-8	2007	On the other hand, the coexpressed UGT1A1 increased Km and decreased the Vmax of the propofol O-glucuronide formation catalyzed by UGT1A9.	o-glucuronide	94-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
17347060-1	2007	BACKGROUND AND AIM: To clarify the precise mode of inheritance of Gilbert syndrome, an unconjugated familial hyperbilirubinemia, where impaired bilirubin conjugation is caused by reduced UGT1A1 activity determined by a defective function of the A(TA)6TAA promoter region of the UGT1A1 gene.	Bilirubin	114-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17220234-9	2007	Tranilast glucuronosyltransferase activity was strongly inhibited by bilirubin, a typical UGT1A1 substrate, and N-3, indicating that the phase I metabolite could affect the tranilast glucuronosyltransferase activity.	Bilirubin	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
17347060-1	2007	BACKGROUND AND AIM: To clarify the precise mode of inheritance of Gilbert syndrome, an unconjugated familial hyperbilirubinemia, where impaired bilirubin conjugation is caused by reduced UGT1A1 activity determined by a defective function of the A(TA)6TAA promoter region of the UGT1A1 gene.	Bilirubin	114-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	278-284
17374650-0	2007	UGT1A1 polymorphism is associated with serum bilirubin concentrations in a randomized, controlled, fruit and vegetable feeding trial.	Bilirubin	45-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17374650-1	2007	UDP-glucuronosyltransferase (UGT) 1A1 glucuronidates bilirubin, estrogens, and exogenous compounds, including dietary carcinogens.	Bilirubin	53-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
17374650-2	2007	The UGT1A1*28 polymorphism, characterized by variation in the number of thymine-adenine repeats in the promoter region, modulates UGT1A1 transcription.	thymine-adenine	72-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
17374650-2	2007	The UGT1A1*28 polymorphism, characterized by variation in the number of thymine-adenine repeats in the promoter region, modulates UGT1A1 transcription.	thymine-adenine	72-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
17496722-2	2007	The most common genotype of Gilbert"s syndrome is the homozygous polymorphism, A(TA)7TAA, in the promoter of the gene for UDP-glucuronosyltransferase 1A1 (UGT1A1), with a thymine adenine insertion in the TATA-box-like sequence, which results in a decrease in UGT1A1 activity.	thymine adenine	171-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-153
17496722-2	2007	The most common genotype of Gilbert"s syndrome is the homozygous polymorphism, A(TA)7TAA, in the promoter of the gene for UDP-glucuronosyltransferase 1A1 (UGT1A1), with a thymine adenine insertion in the TATA-box-like sequence, which results in a decrease in UGT1A1 activity.	thymine adenine	171-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
17496722-2	2007	The most common genotype of Gilbert"s syndrome is the homozygous polymorphism, A(TA)7TAA, in the promoter of the gene for UDP-glucuronosyltransferase 1A1 (UGT1A1), with a thymine adenine insertion in the TATA-box-like sequence, which results in a decrease in UGT1A1 activity.	thymine adenine	171-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	259-265
17151191-0	2007	UDP-glucuronosyltransferase 1A1 is the principal enzyme responsible for etoposide glucuronidation in human liver and intestinal microsomes: structural characterization of phenolic and alcoholic glucuronides of etoposide and estimation of enzyme kinetics.	Etoposide	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
17196409-2	2007	The causative mutation in Caucasians is almost exclusively a TA dinucleotide insertion in the TATA box of the UGT1A1 promoter.	Dinucleoside Phosphates	64-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
17471158-3	2007	This results in a reduced UGT 1A1 expression with 70% less glucuronidation capacity for bilirubin and other UGT1A1 substrates.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-33
17471158-6	2007	The anticancer agent irinotecan is metabolized to the active SN-38, which is further glucuronidated and detoxified by UGT 1A1.	Irinotecan	21-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-125
17471158-6	2007	The anticancer agent irinotecan is metabolized to the active SN-38, which is further glucuronidated and detoxified by UGT 1A1.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-125
17259171-3	2007	When human HepG2 cells were treated with the prooxidants tert-butylhydroquinone and beta-naphthoflavone, cellular UGT1A1 glucuronidation activities were increased.	2-tert-butylhydroquinone	57-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
17259171-3	2007	When human HepG2 cells were treated with the prooxidants tert-butylhydroquinone and beta-naphthoflavone, cellular UGT1A1 glucuronidation activities were increased.	beta-Naphthoflavone	84-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
17259171-8	2007	Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene.	Phenobarbital	249-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
17259171-8	2007	Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene.	Phenobarbital	249-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	302-308
16897040-8	2007	Phenolphthalein, a substrate for UGT1A9, inhibited DL glucuronidation in HLM competitively (K (i) = 0.356 mM), but bilirubin, a substrate for UGT1A1, did not.	Phenolphthalein	0-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
17531109-0	2007	Reversible grade 4 hyperbilirubinemia in a patient with UGT1A1 7/7 genotype treated with irinotecan and cetuximab.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
17531109-5	2007	This case outlines the possibility of severe hepatic toxicity with moderate doses of irinotecan in patients with a UGT1A1 7/7 genotype.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
17151191-0	2007	UDP-glucuronosyltransferase 1A1 is the principal enzyme responsible for etoposide glucuronidation in human liver and intestinal microsomes: structural characterization of phenolic and alcoholic glucuronides of etoposide and estimation of enzyme kinetics.	Glucuronides	194-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
17151191-0	2007	UDP-glucuronosyltransferase 1A1 is the principal enzyme responsible for etoposide glucuronidation in human liver and intestinal microsomes: structural characterization of phenolic and alcoholic glucuronides of etoposide and estimation of enzyme kinetics.	Etoposide	210-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
17151191-3	2007	In vitro UDP-glucuronosyltransferase (UGT) reaction screening with 12 recombinant human UGTs demonstrated that etoposide glucuronidation is mainly catalyzed by UGT1A1.	Etoposide	111-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
17151191-4	2007	Although UGT1A8 and 1A3 also catalyzed the glucuronidation of etoposide, their activities were approximately 10 and 1% of UGT1A1.	Etoposide	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
17151191-9	2007	The data indicated that UGT1A1 is principally responsible for the formation of etoposide glucuronides, mainly in the form of phenolic glucuronide, suggesting that etoposide can be used as a highly selective probe substrate for human UGT1A1 in vitro.	etoposide glucuronide	79-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
17245571-4	2007	RESULTS: Among the UGT isozymes investigated, UGT1A1, 1A3, 1A9, and 2B7 showed glucuronidation activity for indomethacin, with UGT1A9 possessing the highest activity, followed by UGT2B7.	Indomethacin	108-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
17151191-9	2007	The data indicated that UGT1A1 is principally responsible for the formation of etoposide glucuronides, mainly in the form of phenolic glucuronide, suggesting that etoposide can be used as a highly selective probe substrate for human UGT1A1 in vitro.	etoposide glucuronide	79-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	233-239
17151191-9	2007	The data indicated that UGT1A1 is principally responsible for the formation of etoposide glucuronides, mainly in the form of phenolic glucuronide, suggesting that etoposide can be used as a highly selective probe substrate for human UGT1A1 in vitro.	Glucuronides	89-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
17151191-9	2007	The data indicated that UGT1A1 is principally responsible for the formation of etoposide glucuronides, mainly in the form of phenolic glucuronide, suggesting that etoposide can be used as a highly selective probe substrate for human UGT1A1 in vitro.	Etoposide	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
17151191-9	2007	The data indicated that UGT1A1 is principally responsible for the formation of etoposide glucuronides, mainly in the form of phenolic glucuronide, suggesting that etoposide can be used as a highly selective probe substrate for human UGT1A1 in vitro.	Etoposide	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	233-239
17273745-1	2007	The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA).	Fluorouracil	323-337	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17273745-1	2007	The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA).	Fluorouracil	339-343	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17273745-1	2007	The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA).	Irinotecan	350-360	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17273745-1	2007	The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA).	Oxaliplatin	364-375	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17273745-1	2007	The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA).	Oxaliplatin	377-380	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17259247-0	2007	A combinatorial haplotype of the UDP-glucuronosyltransferase 1A1 gene (#60-#IB) increases total bilirubin concentrations in Japanese volunteers.	Bilirubin	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-64
17166930-7	2007	We investigated the frequency of promoter region [thymine-adenine(TA)]7 polymorphism in UGT1A1 gene.	thymine-adenine	50-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
17108060-14	2007	The induction effect of catechins on UGT1A1 seems to be modest and highly variable.	Catechin	24-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
17256720-1	2007	UNLABELLED: The flavonoid chrysin is an important dietary substance and induces UGT1A1 protein expression in cell culture.	Flavonoids	16-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
17256720-2	2007	As a representative of the class of dietary flavonoids, clinical investigations have been considered as a means of inducing hepatic UGT1A1 expression.	Flavonoids	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
17256720-5	2007	However, key differences in Ah receptor recognition and activation of UGT1A1 by chrysin exist when compared with classical mechanisms of UGT1A1 induction by TCDD.	Polychlorinated Dibenzodioxins	157-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
17410034-3	2007	Genetic polymorphisms in the UGT1A1 gene have been identified as one of the causes of the increased diarrhea seen in white patients treated with irinotecan when compared with Japanese patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
17166930-7	2007	We investigated the frequency of promoter region [thymine-adenine(TA)]7 polymorphism in UGT1A1 gene.	Tantalum	66-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
17148966-2	2007	Polymorphisms at the uridin-glucoronosyl-transferase 1A1 (UGT1A1) and multidrug resistance 1 (MDR1) genes may influence, respectively, bilirubin and ATV plasma concentrations.	Bilirubin	135-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-56
17484518-6	2007	Docking of UDP-glucuronic acid to a model of UGT1A1 resulted in a root mean square deviation of only 0.37 angstroms vs. UDP co-crystallized with the plant UGT71G1 template.	Uridine Diphosphate Glucuronic Acid	11-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
17484518-6	2007	Docking of UDP-glucuronic acid to a model of UGT1A1 resulted in a root mean square deviation of only 0.37 angstroms vs. UDP co-crystallized with the plant UGT71G1 template.	Uridine Diphosphate	11-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
17484518-7	2007	The significance of a comparative model generated for UGT1A1 with respect to both the sugar donor and aglycone binding sites, and mechanism, is discussed.	Sugars	86-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
17484518-7	2007	The significance of a comparative model generated for UGT1A1 with respect to both the sugar donor and aglycone binding sites, and mechanism, is discussed.	CHEBI:166892	102-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
17148966-2	2007	Polymorphisms at the uridin-glucoronosyl-transferase 1A1 (UGT1A1) and multidrug resistance 1 (MDR1) genes may influence, respectively, bilirubin and ATV plasma concentrations.	Bilirubin	135-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
17148966-2	2007	Polymorphisms at the uridin-glucoronosyl-transferase 1A1 (UGT1A1) and multidrug resistance 1 (MDR1) genes may influence, respectively, bilirubin and ATV plasma concentrations.	Atazanavir Sulfate	149-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-56
17148966-2	2007	Polymorphisms at the uridin-glucoronosyl-transferase 1A1 (UGT1A1) and multidrug resistance 1 (MDR1) genes may influence, respectively, bilirubin and ATV plasma concentrations.	Atazanavir Sulfate	149-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
17187418-0	2007	Regulation of the UGT1A1 bilirubin-conjugating pathway: role of a new splicing event at the UGT1A locus.	Bilirubin	25-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
17185998-2	2007	Life-threatening diarrhea is observed in up to 25% of patients receiving irinotecan and has been related with irinotecan pharmacokinetics and UGT1A1 genotype status.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
17185998-10	2007	As the association was seen in patients not genetically predisposed at risk for diarrhea due to UGT1A1*28, confirmatory studies of the relationships of ABCC2 genotypes and irinotecan disposition and toxicity are warranted.	Irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
19356014-0	2007	ABCB1, SLCO1B1 and UGT1A1 gene polymorphisms are associated with toxicity in metastatic colorectal cancer patients treated with first-line irinotecan.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
17185519-4	2006	The irinotecan/UGT1A1 issue and the development of molecular diagnostic testing are now to be translated into clinical practice.	Irinotecan	4-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17264799-1	2007	BACKGROUND: Glucuronidation by the UDP glucuronosyltransferase 1A enzymes (UGT1As) is a major pathway for elimination of drugs and endogenous substances, such as bilirubin.	Bilirubin	162-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-65
17184208-1	2006	Depending upon the UDP glucuronosyltransferase 1A1 (UGT1A1) genotype, patients are more or less susceptible to the risk of severe toxicity of irinotecan.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-50
17184208-1	2006	Depending upon the UDP glucuronosyltransferase 1A1 (UGT1A1) genotype, patients are more or less susceptible to the risk of severe toxicity of irinotecan.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
17184208-2	2006	As the US FDA-approved label of irinotecan (CPT-11, Camptosar) has been recently revised to include UGT1A1 genotype among potential risk factors for toxicity, it is expected that UGT1A1 genotyping will be increasingly used in patients undergoing irinotecan treatment.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
17090741-5	2006	The labeling of irinotecan was recently changed and now includes a warning of greater neutropenia risk in patients with reduced activity in the drug-metabolizing enzyme uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-216
17090741-5	2006	The labeling of irinotecan was recently changed and now includes a warning of greater neutropenia risk in patients with reduced activity in the drug-metabolizing enzyme uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	218-224
17090741-7	2006	Numerous studies have demonstrated the effects of genetic factors, especially UGT1A1*28, that contribute to interpatient variability in irinotecan pharmacokinetics and toxicity.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
17090741-8	2006	Irinotecan"s new labeling recommends that clinicians consider reducing the dosage of irinotecan in patients homozygous for UGT1A1*28.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
17090741-8	2006	Irinotecan"s new labeling recommends that clinicians consider reducing the dosage of irinotecan in patients homozygous for UGT1A1*28.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
17090741-9	2006	CONCLUSION: At least part of the interpatient variability of irinotecan toxicity can be explained by the UGT1A1*28 polymorphism.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
17090741-10	2006	Patients who are homozygous for the UGT1A1*28 allele have an increased risk of developing severe neutropenia when receiving irinotecan, especially the 300-350- mg/m2 regimen.	Irinotecan	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
17185519-1	2006	This article focuses on pharmacogenetic associations between genetic polymorphism of uridine diphosphate glucuronosyltransferase (UGT) 1A1 gene and irinotecan toxicity.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-138
17185519-3	2006	On the basis of these backgrounds, the irinotecan label was updated in 2005 in the United States to provide pharmacogenetic information, and a dose reduction of irinotecan should be considered for patients known to be homozygous for the UGT1A1*28 allele when administered in combination with other agents or a single agent.	Irinotecan	161-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	237-243
17192505-3	2007	This analysis extended the work of a previous study that examined the effect of UGT1A1 genotypes on the incidence of severe neutropenia in 86 advanced cancer patients following irinotecan treatment.	Irinotecan	177-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
17192505-7	2007	Based on these findings and other reports, the irinotecan label was modified to indicate the role of UGT1A1*28 polymorphism in the metabolism of irinotecan and the associated increased risk of severe neutropenia.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
17192505-7	2007	Based on these findings and other reports, the irinotecan label was modified to indicate the role of UGT1A1*28 polymorphism in the metabolism of irinotecan and the associated increased risk of severe neutropenia.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
17192505-8	2007	The label modifications also included recommendations for lower starting doses of irinotecan in patients homozygous for the UGT1A1*28 (7/7) polymorphism.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
17164591-6	2007	Patients who have UGT1A6*2 without UGT1A1*28 showed a significant, lower area under concentration-time curve (AUC(0)--&gt;infinity) of PCM, PCM-glucuronide and PCM-sulfate than those of the patients with wild-type UGT1A1 and UGT1A6 (p &lt; 0.05).	acetaminophen glucuronide	140-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
17164591-6	2007	Patients who have UGT1A6*2 without UGT1A1*28 showed a significant, lower area under concentration-time curve (AUC(0)--&gt;infinity) of PCM, PCM-glucuronide and PCM-sulfate than those of the patients with wild-type UGT1A1 and UGT1A6 (p &lt; 0.05).	acetaminophen sulfate ester	160-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
17090120-5	2006	Supersomes containing human UGT1A1 and 1A3 exclusively generated the phenolic glucuronide, albeit with very low activities, whereas UGT1A9 catalyzed the specific formation of the alcoholic glucuronide and UGT2B7 the predominant formation of the phenolic glucuronide with high activities.	Glucuronides	78-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-42
17090120-5	2006	Supersomes containing human UGT1A1 and 1A3 exclusively generated the phenolic glucuronide, albeit with very low activities, whereas UGT1A9 catalyzed the specific formation of the alcoholic glucuronide and UGT2B7 the predominant formation of the phenolic glucuronide with high activities.	Glucuronides	189-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-42
17090120-5	2006	Supersomes containing human UGT1A1 and 1A3 exclusively generated the phenolic glucuronide, albeit with very low activities, whereas UGT1A9 catalyzed the specific formation of the alcoholic glucuronide and UGT2B7 the predominant formation of the phenolic glucuronide with high activities.	Glucuronides	189-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-42
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	204-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	204-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-0	2006	Pharmacogenetic impact of polymorphisms in the coding region of the UGT1A1 gene on SN-38 glucuronidation in Japanese patients with cancer.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	204-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-1	2006	Pharmacogenetic testing for UDP-glucuronosyltransferase (UGT) 1A1*28, a promoter variant of the UGT1A1 gene, is now carried out clinically to estimate the risk of irinotecan-associated toxicity.	Irinotecan	163-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-1	2006	Pharmacogenetic testing for UDP-glucuronosyltransferase (UGT) 1A1*28, a promoter variant of the UGT1A1 gene, is now carried out clinically to estimate the risk of irinotecan-associated toxicity.	Irinotecan	163-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	174-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	186-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	7-ethyl-10-hydroxycamptothecin glucuronide	204-221	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	157-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-11	2006	Concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, altered the disposition of irinotecan remarkably, potentially increasing susceptibility to toxicity.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
16965601-11	2006	Concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, altered the disposition of irinotecan remarkably, potentially increasing susceptibility to toxicity.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
16965601-13	2006	UGT1A1 polymorphisms in the coding region of the UGT1A1 gene should be genotyped in addition to testing for UGT1A1*28 to more accurately predict irinotecan-related toxicity, at least in Asian patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16965601-13	2006	UGT1A1 polymorphisms in the coding region of the UGT1A1 gene should be genotyped in addition to testing for UGT1A1*28 to more accurately predict irinotecan-related toxicity, at least in Asian patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-13	2006	UGT1A1 polymorphisms in the coding region of the UGT1A1 gene should be genotyped in addition to testing for UGT1A1*28 to more accurately predict irinotecan-related toxicity, at least in Asian patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
17315542-13	2006	The formation of DRF-6574 glucuronide by human liver, intestinal and UGT1A1, 1A3 and 1A8 microsomes was effectively inhibited by phenylbutazone.	Glucuronides	26-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
17058217-1	2006	Gilbert"s disease leads to intermittent non-hemolytic hyperbilirubinemia by a reduction of hepatic bilirubin glucuronidation associated with the presence of the UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism.	Bilirubin	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-198
17058217-9	2006	Homozygous combinations of UGT1A1*28 with the other variants increased from 7.4% (normal bilirubin to 42 micromol/L) to 41% to 46.1% (43 to &gt;85 micromol/L), and 100% (&gt;85 micromol/L).	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
29788595-0	2006	Novel personalized medicine technology: UGT1A1 testing for irinotecan as a case study.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
29788595-1	2006	Third Wave"s Invader  UDP glucuronosyltransferase 1A1 (UGT1A1) Molecular Assay, a genotyping system to predict adverse drug reactions in patients receiving the chemotherapeutic agent irinotecan (Camptosar , Pzifer, NY, USA) for the treatment of metastatic colorectal cancer (mCRC), was recently approved by the US FDA.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-53
29788595-1	2006	Third Wave"s Invader  UDP glucuronosyltransferase 1A1 (UGT1A1) Molecular Assay, a genotyping system to predict adverse drug reactions in patients receiving the chemotherapeutic agent irinotecan (Camptosar , Pzifer, NY, USA) for the treatment of metastatic colorectal cancer (mCRC), was recently approved by the US FDA.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
29788595-1	2006	Third Wave"s Invader  UDP glucuronosyltransferase 1A1 (UGT1A1) Molecular Assay, a genotyping system to predict adverse drug reactions in patients receiving the chemotherapeutic agent irinotecan (Camptosar , Pzifer, NY, USA) for the treatment of metastatic colorectal cancer (mCRC), was recently approved by the US FDA.	Irinotecan	195-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
29788595-3	2006	This descriptive analysis highlight these data and the issues for the translation of this test to practice, including gaps in the evidence base, issues regarding adoption of the test to clinical practice and the potential societal impact of UGT1A1 testing for irinotecan prescribing.	Irinotecan	260-270	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	241-247
16982469-3	2006	Recent FDA approval of genetic testing for mutations in the UGT1A1 gene that predict adverse reactions to irinotecan is ushering in a new era that will increasingly rely on genotyping to individualize treatment decisions for patients with cancer as well as for patients at high risk who may be candidates for chemoprevention agents.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	doxifluridine	151-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	doxifluridine	151-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Fluorouracil	396-400	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Fluorouracil	396-400	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17009167-13	2006	Furthermore, we show that after deglycosylation, the resulting aglycone is metabolized in trans-resveratrol-3-O-ss-glucuronide and to a lesser extent in trans-resveratrol-4"-O-ss-glucuronide, and that UGT1A1 is mainly involved in this metabolism.	CHEBI:166892	63-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
17315542-13	2006	The formation of DRF-6574 glucuronide by human liver, intestinal and UGT1A1, 1A3 and 1A8 microsomes was effectively inhibited by phenylbutazone.	Phenylbutazone	129-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
16791115-1	2006	OBJECTIVE: The aim of the study was to investigate relationships among indinavir, lamivudine-triphosphate, and zidovudine-triphosphate pharmacokinetics and pharmacodynamics with polymorphisms in CYP3A5, MDR1, MRP2, MRP4, BCRP, and UGT1A1 genes.	zidovudine triphosphate	111-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	231-237
16545899-4	2006	7-Ethyl-10-hydroxycamptothecin (SN-38) glucuronidation, used as a probe for UGT1A1, showed sigmoidal kinetics with a Hill coefficient (n) of 1.2-1.3 in control and BNF-pretreated HepG2 cells.	Irinotecan	0-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
16545899-4	2006	7-Ethyl-10-hydroxycamptothecin (SN-38) glucuronidation, used as a probe for UGT1A1, showed sigmoidal kinetics with a Hill coefficient (n) of 1.2-1.3 in control and BNF-pretreated HepG2 cells.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
16951398-12	2006	It is suggested that the UGT1A1*28 genotype status could be used as a screening tool for a priori prevention of irinotecan-induced delayed-type diarrhea.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16791115-11	2006	Bilirubin increases were 2-fold higher in UGT1A1 [TA]7/[TA]7 genotypes.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16809730-0	2006	The role of UGT1A1*28 polymorphism in the pharmacodynamics and pharmacokinetics of irinotecan in patients with metastatic colorectal cancer.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
16595709-10	2006	Despite limitations resulting from sample size, results indicate that UGT1A9 I399 and -118T(9/10) may represent additional candidates in combination with UGT1A1 promoter haplotypes for the prediction of SN-38 glucuronidation profile in vivo.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
16595710-2	2006	Incubation of the DHT monoglucuronide with 12 cDNA-expressed recombinant human UGT isoforms and uridine 5"-diphosphoglucuronic acid resulted in a low but measurable DHT diglucuronidation activity primarily with UGT1A8, a gastrointestinal UGT, and to a lesser extent with UGT1A1 and UGT1A9.	dht monoglucuronide	18-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
16595710-2	2006	Incubation of the DHT monoglucuronide with 12 cDNA-expressed recombinant human UGT isoforms and uridine 5"-diphosphoglucuronic acid resulted in a low but measurable DHT diglucuronidation activity primarily with UGT1A8, a gastrointestinal UGT, and to a lesser extent with UGT1A1 and UGT1A9.	5"-diphosphoglucuronic acid	104-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
16595710-2	2006	Incubation of the DHT monoglucuronide with 12 cDNA-expressed recombinant human UGT isoforms and uridine 5"-diphosphoglucuronic acid resulted in a low but measurable DHT diglucuronidation activity primarily with UGT1A8, a gastrointestinal UGT, and to a lesser extent with UGT1A1 and UGT1A9.	Dihydrotestosterone	18-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	271-277
16824027-0	2006	Screening for adverse reactions to irinotecan treatment using the Invader UGT1A1 Molecular Assay.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
16824027-1	2006	Accumulating evidence provides support for the idea that determination of UGT1A1 polymorphisms before irinotecan (CPT-11) treatment is clinically useful and important for predicting and avoiding related toxicities.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
16824027-1	2006	Accumulating evidence provides support for the idea that determination of UGT1A1 polymorphisms before irinotecan (CPT-11) treatment is clinically useful and important for predicting and avoiding related toxicities.	Irinotecan	114-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
16824027-3	2006	A dose reduction of irinotecan should be considered for patients known to be homozygous for the UGT1A1*28 allele when administered in combination with other agents or as a single agent.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
16824027-6	2006	This newly developed method for detecting UGT1A1 polymorphisms is feasible and has the potential to be widely used for rapid and accurate screening before irinotecan treatment.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16809730-1	2006	PURPOSE: UGT1A1*28 polymorphism has been associated with decreased glucuronidation of SN38, the active metabolite of irinotecan.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
16809730-11	2006	In particular, the possibility of a dose reduction for irinotecan in patients with a UGT1A1*28 polymorphism is not supported by the result of this analysis.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16783480-6	2006	The glucuronidation activity of niflumic acid in microsomes from eight human livers significantly correlated with UGT1A1-catalyzed estradiol 3beta-glucuronidation activity (r=0.78, p&lt;0.05).	Niflumic Acid	32-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
16783480-6	2006	The glucuronidation activity of niflumic acid in microsomes from eight human livers significantly correlated with UGT1A1-catalyzed estradiol 3beta-glucuronidation activity (r=0.78, p&lt;0.05).	Estradiol	131-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
16783480-8	2006	CONCLUSIONS: These findings indicate that UGT1A1 is the main isozyme involved in the glucuronidation of niflumic acid in the human liver.	Niflumic Acid	104-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16713428-4	2006	Essentially, microsomal assays with UGT1A1 produced only one of the 2 N-glucuronides, whereas UGT1A9 is capable of forming both N-glucuronides.	n-glucuronides	70-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
16504606-0	2006	Evaluation of mutation effects on UGT1A1 activity toward 17beta-estradiol using liquid chromatography-tandem mass spectrometry.	Estradiol	57-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
16504606-1	2006	Mutations in the gene encoding UDP-glucuronosyltransferase 1A1 (UGT1A1) may reduce the glucuronidation of estradiol, bilirubin, etc.	Estradiol	106-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-62
16504606-1	2006	Mutations in the gene encoding UDP-glucuronosyltransferase 1A1 (UGT1A1) may reduce the glucuronidation of estradiol, bilirubin, etc.	Estradiol	106-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16504606-1	2006	Mutations in the gene encoding UDP-glucuronosyltransferase 1A1 (UGT1A1) may reduce the glucuronidation of estradiol, bilirubin, etc.	Bilirubin	117-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-62
16504606-1	2006	Mutations in the gene encoding UDP-glucuronosyltransferase 1A1 (UGT1A1) may reduce the glucuronidation of estradiol, bilirubin, etc.	Bilirubin	117-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16504606-2	2006	In the present study, we used a liquid chromatography-tandem mass spectrometry (LC/MS/MS) method to assay the activities of recombinant mutated UGT1A1 toward 17beta-estradiol (E2), by determining its glucuronide (E2G) content.	Glucuronides	200-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
16713428-5	2006	The rates of metabolism for UGT1A9, human liver microsomes, and UGT1A1 were 200, 100, and 100 pmol N-glucuronide per minute per milligram of protein, respectively.	n-glucuronide	99-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16685247-0	2006	Invader UGT1A1 molecular assay for irinotecan toxicity.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
16817017-1	2006	During the course of the study of UGT1A1 induction by bilirubin, we could not detect the induction of the reporter gene (-3174/+14) of human UGT1A1 in HepG2 by bilirubin (Mol.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
16817017-4	2006	In this report, we show the finding of the induction of the reporter gene of UGT1A1 by cortisol at 1 microM, a major natural cortico-steroid, with human glucocorticoid receptor (GR).	Hydrocortisone	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
16636344-11	2006	CONCLUSION: These findings suggest that UGT1A1*6 and UGT1A9*22 genotypes may be important for SN-38 glucuronidation and associate with irinotecan-related severe toxicity.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
16636344-11	2006	CONCLUSION: These findings suggest that UGT1A1*6 and UGT1A9*22 genotypes may be important for SN-38 glucuronidation and associate with irinotecan-related severe toxicity.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
16636344-12	2006	Specifically, UGT1A1*6 might be useful for predicting tumor response and survival outcome of Korean patients with NSCLC treated with irinotecan-based chemotherapy.	Irinotecan	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
16682733-4	2006	For example, pharmacogenetic tests currently used in cancer therapy, such as genotyping UGT1A1 to reduce the incidence of severe toxicity of irinotecan and sequencing epidermal growth factor receptor from tumors to identify somatic mutations conferring sensitivity to tyrosine kinase inhibitors, were developed without initial identification of interpopulation differences.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
16821585-4	2006	RESULTS: Three independent lines of enquiry indicated that, in the tumour specimens, SN-38 was glucuronidated primarily by UGT1A1, the isozyme generally recognised as being responsible for hepatic detoxification of this compound, while with NU/ICRF 505 two candidate isoforms emerged - UGT1A8 and/or UGT1A10 - both of which are not normally expressed in the liver.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
16628735-3	2006	UGT1A1 promoter polymorphism is associated both with unconjugated bilirubin level and elevated risk for cholelithiasis in such subset.	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16641252-4	2006	An assay is available for genotypic testing of the enzyme UGT1A1, which is predictive of toxicity from irinotecan.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
16477579-6	2006	Among the UDP-glucuronosyltransferases (UGT) that are known to be expressed in the GI tract, the isoforms UGT1A1, 1A6, 1A8, 1A9 and 1A10 were active in glucuronidating trans- and/or cis-resveratrol.	trans- and/	168-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
16477579-6	2006	Among the UDP-glucuronosyltransferases (UGT) that are known to be expressed in the GI tract, the isoforms UGT1A1, 1A6, 1A8, 1A9 and 1A10 were active in glucuronidating trans- and/or cis-resveratrol.	Resveratrol	182-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
16402080-1	2006	Retigabine (RGB) is an investigational antiepileptic drug, which undergoes extensive UGT1A1, 1A9 and 1A4-mediated N-glucuronidation and N-acetylation.	ezogabine	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16402080-1	2006	Retigabine (RGB) is an investigational antiepileptic drug, which undergoes extensive UGT1A1, 1A9 and 1A4-mediated N-glucuronidation and N-acetylation.	Nitrogen	114-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16513445-8	2006	Intestinal expression of UGT1A1, ABCB1, and ABCC2 was inversely correlated with the effects of ezetimibe on plant sterol serum concentrations.	Sterols	114-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16715376-9	2006	Incubations with various cDNA-expressed UDP-glucuronosyltransferases indicated that the isozymes UGT1A1, UGT1A6, UGT1A8, and UGT1A9 were responsible for glucuronidation of 8-PN.	8-prenylnaringenin	172-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
16610035-1	2006	AIM: To identify the variants in UDP-glucuronosyltransferase 1 (UGT1A1) gene in Gilbert"s syndrome (GS) and to estimate the association between homozygosity for TA insertion and GS in India, as well as the frequency of TA insertion and its impact among normal controls in India.	Tantalum	161-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16610035-1	2006	AIM: To identify the variants in UDP-glucuronosyltransferase 1 (UGT1A1) gene in Gilbert"s syndrome (GS) and to estimate the association between homozygosity for TA insertion and GS in India, as well as the frequency of TA insertion and its impact among normal controls in India.	Tantalum	219-221	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16610035-5	2006	Functional assessment of a novel trinucleotide insertion was done by in silico analysis and by estimating UGT1A1 promoter activity carried out by luciferase reporter assay of appropriate constructs in Hep G2 cell line.	trinucleotide	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
16597364-5	2006	UGT1A1 and UGT1A9 were predominantly responsible for the formation of the 3-O-glucuronide (Km = 149 microM) and 4"-O-glucuronide (Km = 365 microM), respectively.	3-o-glucuronide	74-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16597364-5	2006	UGT1A1 and UGT1A9 were predominantly responsible for the formation of the 3-O-glucuronide (Km = 149 microM) and 4"-O-glucuronide (Km = 365 microM), respectively.	4"-o-glucuronide	112-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16597364-7	2006	Resveratrol was co-incubated with substrates of UGT1A1 (bilirubin and 7-ethyl-10-hydroxycamptothecin (SN-38)) and UGT1A9 (7-hydroxytrifluoromethyl coumarin (7-HFC)).	Resveratrol	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
16597364-10	2006	Hence, resveratrol has the potential to inhibit the glucuronidation of concomitantly administered therapeutic drugs or dietary components that are substrates of UGT1A1 and UGT1A9.	Resveratrol	7-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
16456808-1	2006	BACKGROUND: In the current Phase II study, the authors evaluated the association between genomic polymorphic variants in uridine diphosphate glucuronosyl transferase (UGT1A1), methylenetetrahydrofolate reductase (MTHFR), and thymidylate synthase (TS) genes, and the incidence of the adverse effects of irinotecan and raltitrexed in previously heavily treated patients with metastatic colorectal carcinoma.	Irinotecan	302-312	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
16456808-10	2006	CONCLUSIONS: In the current study, UGT1A1 promoter polymorphism was found to be predictive of the risk of diarrhea, emesis, and fatigue caused by chemotherapy with irinotecan and raltitrexed.	Irinotecan	164-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
16456808-10	2006	CONCLUSIONS: In the current study, UGT1A1 promoter polymorphism was found to be predictive of the risk of diarrhea, emesis, and fatigue caused by chemotherapy with irinotecan and raltitrexed.	raltitrexed	179-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
16456808-11	2006	Screening for UGT1A1 promoter polymorphism may be clinically useful for identifying patients at a higher risk of developing a severe or potentially life-threatening toxicity after irinotecan-based chemotherapy.	Irinotecan	180-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
16513445-7	2006	RESULTS: Up-regulation of intestinal P-gp, MRP2, and UGT1A1 (but not of NPC1L1) by rifampin was associated with markedly decreased areas under the curve of ezetimibe and its glucuronide (116 +/- 78.1 ng.h/mL versus 49.9 +/- 31.0 ng.h/mL and 635 +/- 302 ng.h/mL versus 225 +/- 86.4 ng.h/mL, respectively; both P = .002) and increased intestinal clearances (2400 +/- 1560 mL/min versus 5500 +/- 4610 mL/min [P = .003] and 76.6 +/- 113 mL/min versus 316 +/- 457 mL/min [P = .010], respectively) and nearly abolished sterol-lowering effects.	Rifampin	83-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
16513445-7	2006	RESULTS: Up-regulation of intestinal P-gp, MRP2, and UGT1A1 (but not of NPC1L1) by rifampin was associated with markedly decreased areas under the curve of ezetimibe and its glucuronide (116 +/- 78.1 ng.h/mL versus 49.9 +/- 31.0 ng.h/mL and 635 +/- 302 ng.h/mL versus 225 +/- 86.4 ng.h/mL, respectively; both P = .002) and increased intestinal clearances (2400 +/- 1560 mL/min versus 5500 +/- 4610 mL/min [P = .003] and 76.6 +/- 113 mL/min versus 316 +/- 457 mL/min [P = .010], respectively) and nearly abolished sterol-lowering effects.	Glucuronides	174-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
16513445-7	2006	RESULTS: Up-regulation of intestinal P-gp, MRP2, and UGT1A1 (but not of NPC1L1) by rifampin was associated with markedly decreased areas under the curve of ezetimibe and its glucuronide (116 +/- 78.1 ng.h/mL versus 49.9 +/- 31.0 ng.h/mL and 635 +/- 302 ng.h/mL versus 225 +/- 86.4 ng.h/mL, respectively; both P = .002) and increased intestinal clearances (2400 +/- 1560 mL/min versus 5500 +/- 4610 mL/min [P = .003] and 76.6 +/- 113 mL/min versus 316 +/- 457 mL/min [P = .010], respectively) and nearly abolished sterol-lowering effects.	Sterols	513-519	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
16513445-8	2006	Intestinal expression of UGT1A1, ABCB1, and ABCC2 was inversely correlated with the effects of ezetimibe on plant sterol serum concentrations.	Ezetimibe	95-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16609363-0	2006	Relationship between hyperbilirubinaemia and UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphism in adult HIV-infected Thai patients treated with indinavir.	Indinavir	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-76
16609363-0	2006	Relationship between hyperbilirubinaemia and UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphism in adult HIV-infected Thai patients treated with indinavir.	Indinavir	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
16609363-8	2006	Total, conjugated (direct) and unconjugated (indirect) serum bilirubin concentrations increased significantly at 24 weeks of indinavir treatment for all four genotypes, with a trend towards higher levels depending on the number of UGT1A1 mutant alleles; *6/*28 &gt; *6 &gt; *28 &gt; reference.	Indinavir	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	231-237
16609363-9	2006	The hazards ratio (HR) for serious hyperbilirubinaemia (total bilirubin &gt; 2.5 mg/dl) at week 24 was statistically significant only in those patients carrying the UGT1A1*6 (HR 2.87) and UGT1A1*6/*28 (HR 11.42) genotypes.	Bilirubin	40-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
16609363-9	2006	The hazards ratio (HR) for serious hyperbilirubinaemia (total bilirubin &gt; 2.5 mg/dl) at week 24 was statistically significant only in those patients carrying the UGT1A1*6 (HR 2.87) and UGT1A1*6/*28 (HR 11.42) genotypes.	Bilirubin	40-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
16609363-10	2006	The Ki values for indinavir inhibition of UGT1A1 and UGT1A1*6 were 4.1 and 10.7 mumol/l respectively.	Indinavir	18-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16609363-10	2006	The Ki values for indinavir inhibition of UGT1A1 and UGT1A1*6 were 4.1 and 10.7 mumol/l respectively.	Indinavir	18-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
16609363-13	2006	The Ki values determined for indinavir inhibition of UGT1A1 are consistent with an interaction in vivo, with an additive effect in patients with already impaired bilirubin glucuronidation activity.	Indinavir	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
16609363-13	2006	The Ki values determined for indinavir inhibition of UGT1A1 are consistent with an interaction in vivo, with an additive effect in patients with already impaired bilirubin glucuronidation activity.	Bilirubin	162-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
16480962-6	2006	Only UGT1A4 catalyzed the N-linked glucuronidation of 4-HO-TAM among recombinant human UGT isoforms (UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, UGT2B4, UGT2B7, UGT2B15, and UGT2B17) expressed in insect cells.	4-ho-tam	54-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
16610035-8	2006	Many new DNA variants in UGT1A1 gene were discovered, including a trinucleotide (CAT) insertion in the promoter found in a subset (10%) of GS patients, but not among normal controls.	trinucleotide	66-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16610035-10	2006	CONCLUSION: The genetic epidemiology of GS is variable across ethnic groups and the epistatic interactions among UGT1A1 promoter variants modulate bilirubin glucuronidation.	Bilirubin	147-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
16623861-0	2006	Neonatal jaundice and bilirubin UDP-glucuronosyl transferase 1A1 gene polymorphism in Turkish patients.	Bilirubin	22-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-64
16623861-3	2006	The aim of this study was to investigate whether the number of thymine-adenine repeats in the promoter region of UGT-1A1 was related to non-physiologic hyperbilirubinemia of unexplained aetiology in Turkish newborns.	thymine-adenine	63-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-120
16623861-4	2006	These patients (n=106) were genotyped for their thymine-adenine repeat number in the promoter region of UGT-1A1, and were divided into two groups according to their bilirubin level.	thymine-adenine	48-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-111
16267566-5	2006	The absence of bilirubin UDP-glucoronyltransferase (UGT1A1) activity in CN patients causes high serum levels of unconjugated bilirubin and brain damage in infancy.	Bilirubin	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
16557566-4	2006	Our results show that patients with CF and gallstones are significantly more likely to carry at least one Gilbert UGT1A1 allele compared with stone-free patients (OR 7.3; P = .042) and that these carriers display significantly higher serum levels of unconjugated bilirubin (P = .002).	Bilirubin	263-272	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
16551870-0	2006	Irinotecan inactivation is modulated by epigenetic silencing of UGT1A1 in colon cancer.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16551870-2	2006	The UGT1A1-metabolizing enzyme, expressed in liver and colon, is primarily involved in the inactivation of its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	129-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
16551870-2	2006	The UGT1A1-metabolizing enzyme, expressed in liver and colon, is primarily involved in the inactivation of its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	161-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
16551870-5	2006	Bisulfite sequencing of the UGT1A1 gene revealed the aberrant methylation of specific CpG islands in UGT1A1-negative cells.	hydrogen sulfite	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
16551870-5	2006	Bisulfite sequencing of the UGT1A1 gene revealed the aberrant methylation of specific CpG islands in UGT1A1-negative cells.	hydrogen sulfite	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
16551870-9	2006	Loss of UGT1A1 methylation was further associated with an increase in UGT1A1 protein content and with an enhanced inactivation of SN-38 by 300% in HCT-116 cells.	Irinotecan	130-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
16551870-10	2006	CONCLUSIONS: We conclude that DNA methylation represses UGT1A1 expression in colon cancer and that this process may contribute to the level of tumoral inactivation of the anticancer agent SN-38 and potentially influence clinical response.	Irinotecan	188-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16513445-10	2006	CONCLUSIONS: The disposition and sterol-lowering effects of ezetimibe are modified by metabolic degradation of the drug via intestinal UGT1A1 and either intestinal or hepatic secretion (or both) via P-gp and MRP2.	Ezetimibe	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
16877259-5	2006	Although the role of the UGT1A1 *28 genetic variant has received much attention in altered toxicity upon irinotecan treatment, other UGT1A enzymes also play an important role.	Irinotecan	105-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16337205-3	2006	We have constructed a self-inactivating lentiviral vector (LV-ALBUGT) that expresses the human bilirubin UDP-glucuronosyltransferase (UGT1A1) from a liver-specific promoter.	Bilirubin	95-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
16424820-0	2006	Study of the genetic determinants of UGT1A1 inducibility by phenobarbital in cultured human hepatocytes.	Phenobarbital	60-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
16424820-1	2006	UGT1A1 is induced by phenobarbital.	Phenobarbital	21-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16424820-6	2006	Significant induction of UGT1A1 catalytic activity was observed in 82% and 100% of the cultures treated with phenobarbital for 2 days (median fold-induction = 1.6, range 1.3-2.8; n = 28) and 6 days (median fold-induction = 2.8, range 1.6-6.4; n = 16), respectively.	Phenobarbital	109-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16288819-0	2006	Successful treatment of severe unconjugated hyperbilirubinemia via induction of UGT1A1 by rifampicin.	Rifampin	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
17207411-4	2006	UGT1A1 activity has been measured in fluorescent assay using scopoletin as a substrate.	Scopoletin	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16171463-0	2005	Role of cysteine residues in the function of human UDP glucuronosyltransferase isoform 1A1 (UGT1A1).	Cysteine	8-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-90
16849011-1	2006	PURPOSE: It has been reported that carvedilol, which has beta-adrenergic blocking and vasodilating activities, is mainly metabolized by UDP-glucuronosyltransferase (UGT) 1A1, UGT2B4, UGT2B7 and CYP2D6.	Carvedilol	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-173
16849011-8	2006	CONCLUSION: Polymorphisms of UGT1A1, UGT2B7 and CYP2D6 strongly affect the pharmacokinetics and disposition of carvedilol in Japanese.	Carvedilol	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
16171463-7	2005	N-Ethylmaleimide did not inhibit UGT1A1 activity in native microsomes, but prevented UGT1A1 activation by UDP-GlcNAc and inhibited the activity in digitonin-permeabilized microsomes.	Ethylmaleimide	0-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16171463-0	2005	Role of cysteine residues in the function of human UDP glucuronosyltransferase isoform 1A1 (UGT1A1).	Cysteine	8-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
16171463-7	2005	N-Ethylmaleimide did not inhibit UGT1A1 activity in native microsomes, but prevented UGT1A1 activation by UDP-GlcNAc and inhibited the activity in digitonin-permeabilized microsomes.	Uridine Diphosphate N-Acetylglucosamine	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16171463-1	2005	Bilirubin glucuronidation, catalysed by UGT1A1 [UGT (UDP glucuronosyltransferase) isoform 1A1, EC 2.4.1.17], is critical for biliary elimination of bilirubin.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
16171463-9	2005	Together, the results suggested that free thiol groups, but not disulphide bonding, of seven cysteine residues within the intracisternal region of human UGT1A1 are important for its catalytic activity, while cysteine residues in the cytosolic domain may be involved in its physiological activation by UDP-GlcNAc.	Sulfhydryl Compounds	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
16171463-1	2005	Bilirubin glucuronidation, catalysed by UGT1A1 [UGT (UDP glucuronosyltransferase) isoform 1A1, EC 2.4.1.17], is critical for biliary elimination of bilirubin.	Bilirubin	148-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
16171463-9	2005	Together, the results suggested that free thiol groups, but not disulphide bonding, of seven cysteine residues within the intracisternal region of human UGT1A1 are important for its catalytic activity, while cysteine residues in the cytosolic domain may be involved in its physiological activation by UDP-GlcNAc.	Cysteine	93-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
16171463-9	2005	Together, the results suggested that free thiol groups, but not disulphide bonding, of seven cysteine residues within the intracisternal region of human UGT1A1 are important for its catalytic activity, while cysteine residues in the cytosolic domain may be involved in its physiological activation by UDP-GlcNAc.	Cysteine	208-216	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
16171463-3	2005	Nucleotide sequence analysis of UGT1A1 in two CN-1 patients revealed that patient A was homozygous for a nt 530 G--&gt;A (where nt 530 G--&gt;A means guanine to adenine transition at nucleotide 530) mutation, predicting a C177Y substitution, and patient B had a nt 466 T--&gt;C mutation on one allele and a nt 1070 A--&gt;G mutation on the other, predicting a C156R and a Q357R substitution respectively.	Guanine	150-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
16171463-9	2005	Together, the results suggested that free thiol groups, but not disulphide bonding, of seven cysteine residues within the intracisternal region of human UGT1A1 are important for its catalytic activity, while cysteine residues in the cytosolic domain may be involved in its physiological activation by UDP-GlcNAc.	Uridine Diphosphate N-Acetylglucosamine	301-311	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
16171463-3	2005	Nucleotide sequence analysis of UGT1A1 in two CN-1 patients revealed that patient A was homozygous for a nt 530 G--&gt;A (where nt 530 G--&gt;A means guanine to adenine transition at nucleotide 530) mutation, predicting a C177Y substitution, and patient B had a nt 466 T--&gt;C mutation on one allele and a nt 1070 A--&gt;G mutation on the other, predicting a C156R and a Q357R substitution respectively.	Adenine	161-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
16171463-4	2005	All 11 cysteine residues of mature human UGT1A1 are highly conserved in other human UGT isoforms and in rat, mouse and Rhesus monkey UGT1A1, suggesting their functional importance.	Cysteine	7-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
16171463-5	2005	Expression of mutagenized UGT1A1 plasmids showed that substitution of any of the seven cysteine residues located within the endoplasmic reticulum cisternae (including those mutated in patients A and B) abolished UGT1A1 activity or markedly increased its apparent K(m) for bilirubin.	Cysteine	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
16171463-5	2005	Expression of mutagenized UGT1A1 plasmids showed that substitution of any of the seven cysteine residues located within the endoplasmic reticulum cisternae (including those mutated in patients A and B) abolished UGT1A1 activity or markedly increased its apparent K(m) for bilirubin.	Cysteine	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-218
16171463-5	2005	Expression of mutagenized UGT1A1 plasmids showed that substitution of any of the seven cysteine residues located within the endoplasmic reticulum cisternae (including those mutated in patients A and B) abolished UGT1A1 activity or markedly increased its apparent K(m) for bilirubin.	Bilirubin	272-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
16171463-5	2005	Expression of mutagenized UGT1A1 plasmids showed that substitution of any of the seven cysteine residues located within the endoplasmic reticulum cisternae (including those mutated in patients A and B) abolished UGT1A1 activity or markedly increased its apparent K(m) for bilirubin.	Bilirubin	272-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-218
16171463-6	2005	Substitution of the three cysteine residues within the C-terminal cytosolic tail had minimal effect on basal UGT1A1 activity, but prevented UGT1A1 activation by UDP-GlcNAc.	Cysteine	26-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
16171463-6	2005	Substitution of the three cysteine residues within the C-terminal cytosolic tail had minimal effect on basal UGT1A1 activity, but prevented UGT1A1 activation by UDP-GlcNAc.	Uridine Diphosphate N-Acetylglucosamine	161-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
16491625-0	2005	UGT1A1 genotyping in patients undergoing treatment with irinotecan.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16051636-3	2005	It is known that different isoforms of UDP-glucuronosyltransferase (UGT) are involved in E2 glucuronidation: UGT1A1 leads exclusively to the 3-glucuronide and is stimulated by E2 via homotropic kinetics, whereas UGT2B7 gives rise to the 17-glucuronide of E2 following Michaelis-Menten kinetics.	3-glucuronide	141-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
16051636-3	2005	It is known that different isoforms of UDP-glucuronosyltransferase (UGT) are involved in E2 glucuronidation: UGT1A1 leads exclusively to the 3-glucuronide and is stimulated by E2 via homotropic kinetics, whereas UGT2B7 gives rise to the 17-glucuronide of E2 following Michaelis-Menten kinetics.	17-glucuronide	237-251	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
16051636-8	2005	The effect of daidzein on the 3-glucuronidation of E2 in human hepatic microsomes was also obtained with human recombinant UGT1A1.	daidzein	14-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
16267624-0	2005	Pharmacogenetics of irinotecan: a promoter polymorphism of UGT1A1 gene and severe adverse reactions to irinotecan.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
16267624-1	2005	This review focuses on a pharmacogenetic association between genetic polymorphism of UGT1A1 gene and severe adverse reactions to irinotecan.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16267624-4	2005	A case-control study of Japanese cancer patients revealed that those with the variant UGT1A1 alleles were at significantly higher risk of severe adverse reactions to irinotecan, suggesting that the genotyping strategy would be clinically useful.	Irinotecan	166-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
16187975-8	2005	UGT 1A1, 1A3, 1A6, 1A7, 1A8, 1A9, 1A10 and 2B7 glucuronidated naproxen.	Naproxen	62-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-7
16118329-6	2005	By analysis of the double-reciprocal plots of bilirubin glucuronidation activities at different bilirubin concentrations in the presence of fixed concentrations of inhibitors, the UGT1A1 inhibition by atazanavir and indinavir was demonstrated to follow a linear mixed-type inhibition mechanism (Ki = 1.9 and 47.9 microM, respectively).	Bilirubin	46-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
16118329-6	2005	By analysis of the double-reciprocal plots of bilirubin glucuronidation activities at different bilirubin concentrations in the presence of fixed concentrations of inhibitors, the UGT1A1 inhibition by atazanavir and indinavir was demonstrated to follow a linear mixed-type inhibition mechanism (Ki = 1.9 and 47.9 microM, respectively).	Bilirubin	96-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
16118329-6	2005	By analysis of the double-reciprocal plots of bilirubin glucuronidation activities at different bilirubin concentrations in the presence of fixed concentrations of inhibitors, the UGT1A1 inhibition by atazanavir and indinavir was demonstrated to follow a linear mixed-type inhibition mechanism (Ki = 1.9 and 47.9 microM, respectively).	Atazanavir Sulfate	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
16118329-7	2005	These results suggest that a direct inhibition of UGT1A1-mediated bilirubin glucuronidation may provide a mechanism for the reversible hyperbilirubinemia associated with administration of atazanavir as well as indinavir.	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
16118329-7	2005	These results suggest that a direct inhibition of UGT1A1-mediated bilirubin glucuronidation may provide a mechanism for the reversible hyperbilirubinemia associated with administration of atazanavir as well as indinavir.	Atazanavir Sulfate	188-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
16118329-7	2005	These results suggest that a direct inhibition of UGT1A1-mediated bilirubin glucuronidation may provide a mechanism for the reversible hyperbilirubinemia associated with administration of atazanavir as well as indinavir.	Indinavir	210-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
16019265-2	2005	A single injection of pDNA expressing hUGT1A1 under the CMV promoter resulted in excretion of bilirubin glucuronides in bile and a significant decrease in serum bilirubin for at least 2 or 4 weeks, respectively.	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-45
16019265-2	2005	A single injection of pDNA expressing hUGT1A1 under the CMV promoter resulted in excretion of bilirubin glucuronides in bile and a significant decrease in serum bilirubin for at least 2 or 4 weeks, respectively.	Glucuronides	104-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-45
16019265-2	2005	A single injection of pDNA expressing hUGT1A1 under the CMV promoter resulted in excretion of bilirubin glucuronides in bile and a significant decrease in serum bilirubin for at least 2 or 4 weeks, respectively.	Bilirubin	161-170	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-45
16139098-4	2005	Further investigation identified multiple UGT isoforms to be responsible for catalyzing the addition of glucuronic acid to ethanol, with UGT1A1 and 2B7 being the two most prevalent isoforms.	Glucuronic Acid	104-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
16139098-4	2005	Further investigation identified multiple UGT isoforms to be responsible for catalyzing the addition of glucuronic acid to ethanol, with UGT1A1 and 2B7 being the two most prevalent isoforms.	Ethanol	123-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
16139098-5	2005	Co-incubation with bilirubin or 3"-azido-3"-deoxythymidine (UGT1A1 and 2B7 inhibitors, respectively) inhibited the greatest amount of ethyl glucuronide formation, though other UGT inhibitors also showed some effect.	Bilirubin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-74
16139098-5	2005	Co-incubation with bilirubin or 3"-azido-3"-deoxythymidine (UGT1A1 and 2B7 inhibitors, respectively) inhibited the greatest amount of ethyl glucuronide formation, though other UGT inhibitors also showed some effect.	Zidovudine	32-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-74
16139098-5	2005	Co-incubation with bilirubin or 3"-azido-3"-deoxythymidine (UGT1A1 and 2B7 inhibitors, respectively) inhibited the greatest amount of ethyl glucuronide formation, though other UGT inhibitors also showed some effect.	ethyl glucuronide	134-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-74
16187975-11	2005	UGT 1A1, 1A7, 1A9 and 1A10 catalysed both the phenolic and acyl glucuronidation of desmethylnaproxen, while UGT 1A3, 1A6 and 2B7 formed only the acyl glucuronide.	desmethylnaproxen	83-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-7
16187975-11	2005	UGT 1A1, 1A7, 1A9 and 1A10 catalysed both the phenolic and acyl glucuronidation of desmethylnaproxen, while UGT 1A3, 1A6 and 2B7 formed only the acyl glucuronide.	acyl glucuronide	145-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-7
16166450-9	2005	Among the UGT1A isoforms screened, ketoconazole showed the highest inhibitory effect on UGT1A1 and UGT1A9.	Ketoconazole	35-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
16237771-7	2005	The bilirubin levels for the cholelithiasis patients with the homozygous variant-UGT1A1 gene were significantly different from the control analog (18.0+/-6.5 and 12.7+/-2.9 micromol/L, respectively; P&lt;0.001, Student"s t test).	Bilirubin	4-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
16166450-11	2005	CONCLUSIONS: These results show that ketoconazole is a potent UGT1A1 inhibitor, which seems the basis for increased exposure to SN-38 when coadministered with irinotecan.	Ketoconazole	37-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
16166450-11	2005	CONCLUSIONS: These results show that ketoconazole is a potent UGT1A1 inhibitor, which seems the basis for increased exposure to SN-38 when coadministered with irinotecan.	Irinotecan	128-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
16166450-11	2005	CONCLUSIONS: These results show that ketoconazole is a potent UGT1A1 inhibitor, which seems the basis for increased exposure to SN-38 when coadministered with irinotecan.	Irinotecan	159-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
15993909-9	2005	Genes in the conventional AH gene battery (e.g. CYP1A1, CYP1A2, CYP1B1, ALDH3A1, NQO1 and UGT1A1) remain responsive to TCDD in H/W rats despite the large deletion.	Polychlorinated Dibenzodioxins	119-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
16187025-5	2005	The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity.	Irinotecan	77-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
16187025-5	2005	The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
16187025-7	2005	We suggest that irinotecan offers an effective treatment option for children with recurrent brain stem glioma and other genetic variants except UGT1A1 may be a risk factor for irinotecan-induced toxicity.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
15828025-5	2005	The main aim of this review is to provide an overview of the known polymorphisms present in the genes which codify for factors (thymidylate synthase dihydropyrimidine dehydrogenase, uridine diphosphate (UDP)-glucuronosyl-transferase 1A1, enzymes implicated in DNA repair) involved in the action mechanisms of the drugs now utilized in chemotherapeutic treatment of colorectal carcinoma, such as fluoropyrimidines, irinotecan, and platinum agents.	fluoropyrimidines	395-412	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-236
15828025-5	2005	The main aim of this review is to provide an overview of the known polymorphisms present in the genes which codify for factors (thymidylate synthase dihydropyrimidine dehydrogenase, uridine diphosphate (UDP)-glucuronosyl-transferase 1A1, enzymes implicated in DNA repair) involved in the action mechanisms of the drugs now utilized in chemotherapeutic treatment of colorectal carcinoma, such as fluoropyrimidines, irinotecan, and platinum agents.	Irinotecan	414-424	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-236
16092069-4	2005	The identification of the metabolites formed was elucidated using HPLC with diode array detection as well as HPLC/API-ES MS. XN was efficiently glucuronidated by UGT 1 A 8, 1 A 9, and 1 A 10; further important UGTs were UGT 1 A 1, 1 A 7, and 2 B 7.	xanthohumol	125-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	220-229
16076256-0	2005	Single hepatic venous injection of liver-specific naked plasmid vector expressing human UGT1A1 leads to long-term correction of hyperbilirubinemia and prevention of chronic bilirubin toxicity in Gunn rats.	Bilirubin	133-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15986396-8	2005	Using an heterologous expression system, the bilirubin-conjugating UGT1A1 enzyme was identified among all known UGTs (n = 16) as the predominant enzyme involved.	Bilirubin	45-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
16004608-1	2005	PURPOSE: Homozygosity for the (AT)7 allele of uridine diphosphate glucuronosyl transferase 1A (UGT1A1) gene polymorphism is associated with increased bilirubin levels in sickle cell anemia (SCA).	Bilirubin	150-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
16004608-13	2005	CONCLUSIONS: Apart from UGT1A1 (AT)7 homozygosity, Hb F, age and gender are the other factors that significantly influence serum bilirubin level in SCA.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
16083704-7	2005	RESULTS: RIFA enhanced bile acid detoxification as well as bilirubin conjugation and excretion as reflected by enhanced expression of CYP3A4, UGT1A1, and MRP2.	Rifampin	9-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
16076256-3	2005	Although repeat injections of pcDNA3hUGT1A1 consistently reduced serum bilirubin levels, the effect did not exceed 2 weeks; hUGT1A1 was detectable in livers only for 2 weeks, despite the presence of vector and transcript for at least 1 month.	Bilirubin	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-43
16012956-2	2005	Gilbert"s syndrome is recessively inherited, unconjugated hyperbilirubinemia caused by decreased conjugation rate of bilirubin associated mostly with homozygous A(TA) 7 TAA variant of the TATAA-box in the UGT1A1 gene promoter.	Bilirubin	63-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	205-211
15921999-2	2005	Three substrates were chosen to cover both UGT1A and UGT2B family isozymes: bilirubin (substrate of UGT1A1), p-nitrophenol (UGT1A6) and ethinylestradiol (UGT2B1 and 2B3 for position C17 and UGT1A1 for position C3).	Bilirubin	76-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
15930350-8	2005	Patients with UDP-glucuronosyltransferase (UGT1A1; TA)6/6 promoter genotype had a lower ratio of free to glucuronide form of SN-38 than in patients with &gt;/=1 (TA)7 allele.	Glucuronides	105-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
15896333-2	2005	In this study, the effects of sulforaphane (SFN) and its sulfide analog, erucin (ERN), have been examined on the induction of the phase II enzymes, quinine oxidoreductase (NQO1) and UDP-glucuronosyl transferase (UGT1A1), multidrug transporter (MRP2), cell cycle arrest and cell death in human colon adenocarcinoma Caco-2 cells.	sulforaphane	30-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-218
15896333-2	2005	In this study, the effects of sulforaphane (SFN) and its sulfide analog, erucin (ERN), have been examined on the induction of the phase II enzymes, quinine oxidoreductase (NQO1) and UDP-glucuronosyl transferase (UGT1A1), multidrug transporter (MRP2), cell cycle arrest and cell death in human colon adenocarcinoma Caco-2 cells.	sulforaphane	44-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-218
15896333-5	2005	Erucin (20 microM) induced the mRNAs of NQO1, UGT1A1 and MRP2 by 11.1-, 11.6- and 6.7-fold, whereas sulforaphane (20 microM) induced 3.3-, 5.3- and 2.2-fold, respectively.	erucin	0-6	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
15930350-8	2005	Patients with UDP-glucuronosyltransferase (UGT1A1; TA)6/6 promoter genotype had a lower ratio of free to glucuronide form of SN-38 than in patients with &gt;/=1 (TA)7 allele.	Irinotecan	125-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
15716465-11	2005	Its association with variants of the UGT1A1 promoter and UGT1A7 gene may influence irinotecan metabolism.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
15769885-0	2005	Acyl glucuronidation of fluoroquinolone antibiotics by the UDP-glucuronosyltransferase 1A subfamily in human liver microsomes.	Fluoroquinolones	24-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-89
15769885-5	2005	In a bank of human liver microsomes (n = 14), the glucuronidation activities of LVFX, MFLX, and STFX correlated highly with UGT1A1-selective beta-estradiol 3-glucuronidation activity, whereas the glucuronidation activity of GPFX correlated highly with UGT1A9-selective propofol glucuronidation activity.	Moxifloxacin	86-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
15769885-5	2005	In a bank of human liver microsomes (n = 14), the glucuronidation activities of LVFX, MFLX, and STFX correlated highly with UGT1A1-selective beta-estradiol 3-glucuronidation activity, whereas the glucuronidation activity of GPFX correlated highly with UGT1A9-selective propofol glucuronidation activity.	sitafloxacin	96-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
15769885-5	2005	In a bank of human liver microsomes (n = 14), the glucuronidation activities of LVFX, MFLX, and STFX correlated highly with UGT1A1-selective beta-estradiol 3-glucuronidation activity, whereas the glucuronidation activity of GPFX correlated highly with UGT1A9-selective propofol glucuronidation activity.	Propofol	269-277	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
15769885-6	2005	Among 12 recombinant UGT enzymes, UGT1A1, 1A3, 1A7, and 1A9 catalyzed the glucuronidation of these fluoroquinolones.	Fluoroquinolones	99-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
15858133-3	2005	A heterozygous G &gt; A transition at the 5" splicing donor consensus sequence in intron 14 leading to exon 14 skipping (IVS14+1 G &gt; A, DPYD*2A) with partial loss of enzyme activity may be partly responsible for 5FU induced toxicity, whereas irinotecan associated toxicity may in part be explained by an aberrant UGT1A1 promoter (TA)(n) genotype underlying Gilbert"s syndrome with reduced liver glucuronidation activity.	Fluorouracil	215-218	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	316-322
15858133-3	2005	A heterozygous G &gt; A transition at the 5" splicing donor consensus sequence in intron 14 leading to exon 14 skipping (IVS14+1 G &gt; A, DPYD*2A) with partial loss of enzyme activity may be partly responsible for 5FU induced toxicity, whereas irinotecan associated toxicity may in part be explained by an aberrant UGT1A1 promoter (TA)(n) genotype underlying Gilbert"s syndrome with reduced liver glucuronidation activity.	Irinotecan	245-255	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	316-322
15953334-2	2005	A Chinese girl with severe jaundice was recently diagnosed to have CN syndrome type I by analyzing the bilirubin-uridinediphospho (UDP)-glucuronosyltransferase gene (UGT1A1).	Bilirubin	103-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
15716465-2	2005	UGT1A1*28 is a functional UGT promoter polymorphism associated with Gilbert"s disease and severe irinotecan toxicity, which also occurs in the absence of UGT1A1*28.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15988124-4	2005	The TA-1801A glucuronosyltransferase activity in human liver microsomes was inhibited by bilirubin (typical substrate for UGT1A1), propofol (typical substrate for UGT1A9), diclofenac (substrate for UGT1A9 and UGT2B7), and genistein (substrate for UGT1A1, UGT1A3, and UGT1A9).	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
15988124-4	2005	The TA-1801A glucuronosyltransferase activity in human liver microsomes was inhibited by bilirubin (typical substrate for UGT1A1), propofol (typical substrate for UGT1A9), diclofenac (substrate for UGT1A9 and UGT2B7), and genistein (substrate for UGT1A1, UGT1A3, and UGT1A9).	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	247-253
15988124-4	2005	The TA-1801A glucuronosyltransferase activity in human liver microsomes was inhibited by bilirubin (typical substrate for UGT1A1), propofol (typical substrate for UGT1A9), diclofenac (substrate for UGT1A9 and UGT2B7), and genistein (substrate for UGT1A1, UGT1A3, and UGT1A9).	Propofol	131-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	247-253
15988124-5	2005	The inhibition by bilirubin, propofol, and diclofenac of the TA-1801A glucuronidation was less pronounced in jejunum microsomes than liver microsomes, suggesting that the contribution of UGT1A1, UGT1A9, and UGT2B7 to the TA-1801A glucuronidation is smaller in the intestine than the liver.	Bilirubin	18-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
15988124-5	2005	The inhibition by bilirubin, propofol, and diclofenac of the TA-1801A glucuronidation was less pronounced in jejunum microsomes than liver microsomes, suggesting that the contribution of UGT1A1, UGT1A9, and UGT2B7 to the TA-1801A glucuronidation is smaller in the intestine than the liver.	Propofol	29-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
15988124-5	2005	The inhibition by bilirubin, propofol, and diclofenac of the TA-1801A glucuronidation was less pronounced in jejunum microsomes than liver microsomes, suggesting that the contribution of UGT1A1, UGT1A9, and UGT2B7 to the TA-1801A glucuronidation is smaller in the intestine than the liver.	Diclofenac	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
15867280-0	2005	Cruciferae interact with the UGT1A1*28 polymorphism to determine serum bilirubin levels in humans.	Bilirubin	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
15867280-1	2005	UDP-glucuronosyltransferase (UGT) 1A1 is a conjugating biotransformation enzyme that plays a role in maintaining levels of endogenous compounds (e.g., bilirubin) and handling exogenous compounds, including carcinogens.	Bilirubin	151-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
15867280-2	2005	The UGT1A1*28 polymorphism results in decreased UGT1A1 promoter activity due to 7 thymine-adenine (TA) repeats instead of the commonly found 6 repeats.	7 thymine-adenine	80-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
15867280-2	2005	The UGT1A1*28 polymorphism results in decreased UGT1A1 promoter activity due to 7 thymine-adenine (TA) repeats instead of the commonly found 6 repeats.	7 thymine-adenine	80-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
15867280-2	2005	The UGT1A1*28 polymorphism results in decreased UGT1A1 promoter activity due to 7 thymine-adenine (TA) repeats instead of the commonly found 6 repeats.	Tantalum	99-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
15867280-2	2005	The UGT1A1*28 polymorphism results in decreased UGT1A1 promoter activity due to 7 thymine-adenine (TA) repeats instead of the commonly found 6 repeats.	Tantalum	99-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
15867280-8	2005	There was a significant inverse association between all 3 bilirubin measures and interaction of UGT1A1*28 genotype with Cruciferae intake (P &lt; 0.02 for each measure); individuals with the 7/7 genotype had reduced bilirubin concentrations with increased intake of cruciferous vegetables, whereas individuals with the 6/6 or 6/7 genotype did not.	Bilirubin	216-225	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
15867280-9	2005	With regard to UGT1A1-conjugated carcinogens (e.g., heterocyclic amines, polycyclic aromatic hydrocarbons), individuals with decreased UGT1A1 activity due to the 7/7 genotype may be at greater risk for carcinogenesis, but our results imply that they also may have greater opportunity to decrease that risk through dietary intervention.	heterocyclic amines	52-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
15867280-9	2005	With regard to UGT1A1-conjugated carcinogens (e.g., heterocyclic amines, polycyclic aromatic hydrocarbons), individuals with decreased UGT1A1 activity due to the 7/7 genotype may be at greater risk for carcinogenesis, but our results imply that they also may have greater opportunity to decrease that risk through dietary intervention.	Polycyclic Aromatic Hydrocarbons	73-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
15855726-2	2005	Previously, we demonstrated that the glucuronidation of 4"-HPPH is catalyzed by multiple UDP-glucuronosyltransferases (UGTs) of UGT1A1, UGT1A4, UGT1A6, and UGT1A9.	hydroxyphenytoin	56-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
15801936-3	2005	All patients were genotyped for allelic variants in genes encoding drug metabolizing enzymes (CYP3A4, CYP3A5, UGT1A1) and drug transporters (ABCB1, ABCC2 and ABCG2) that are involved in irinotecan disposition.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
15864130-2	2005	SN-38, the active metabolite of the anticancer agent irinotecan, is metabolized by both UGT1A1 and UGT1A9.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15864130-2	2005	SN-38, the active metabolite of the anticancer agent irinotecan, is metabolized by both UGT1A1 and UGT1A9.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15853761-11	2005	Since UGT1A1 metabolizes not only bilirubin but also hormones and drugs, the mutations could be involved in carcinogenesis and adverse drug reactions.	Bilirubin	34-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
15855726-4	2005	In the present study, we investigated the relationship between the extent of interindividual variability in the urinary excretion levels of 4"-HPPH and its O-glucuronide and genotyping of CYP2C9, CYP2C19, UGT1A1, UGT1A6, and UGT1A9.	hydroxyphenytoin	140-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	205-211
15777743-1	2005	UDP-glucuronosyltransferase1A1 (UGT1A1) catalyses glucuronidation of bilirubin (the final break down product of heme which is produced mainly in the spleen and liver) and is located on the lumen of the endoplasmic reticulum (ER).	Bilirubin	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
15777743-1	2005	UDP-glucuronosyltransferase1A1 (UGT1A1) catalyses glucuronidation of bilirubin (the final break down product of heme which is produced mainly in the spleen and liver) and is located on the lumen of the endoplasmic reticulum (ER).	Bilirubin	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
15777743-1	2005	UDP-glucuronosyltransferase1A1 (UGT1A1) catalyses glucuronidation of bilirubin (the final break down product of heme which is produced mainly in the spleen and liver) and is located on the lumen of the endoplasmic reticulum (ER).	Heme	112-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
15777743-1	2005	UDP-glucuronosyltransferase1A1 (UGT1A1) catalyses glucuronidation of bilirubin (the final break down product of heme which is produced mainly in the spleen and liver) and is located on the lumen of the endoplasmic reticulum (ER).	Heme	112-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
15949398-9	2005	The levels of UGT1A1, UGT1A8, and UGT1A10 mRNA expression were significantly increased in the cells treated with 25 micromol/L sulforaphane compared to that in the controls (P = 0.006, P = 0.017, and P = 0.008 respectively).	sulforaphane	127-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
15985997-5	2005	Mutations in the gene encoding bilirubin-UGT (UGT1A1), lead to complete or partial inactivation of the enzyme causing the rare autosomal recessively inherited conditions, Crigler-Najjar syndrome type 1 (CN-1) and type 2 (CN-2).	Bilirubin	31-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
15771689-3	2005	Recently, it was reported that the -3263T &gt; G mutation in the phenobarbital response enhancer module in UGT1A1 was associated with the majority of cases of Gilbert syndrome.	Phenobarbital	65-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
15949398-14	2005	CONCLUSION: (1) Low dose sulforaphane induces the expression of UGT1A, UGT1A1, UGT1A A8, and UGT1A A10 mRNA significantly.	sulforaphane	25-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
15572581-10	2005	The intrinsic clearance of 7-ethyl-10-hydroxycamptothecin (SN-38) by P229L UGT1A1 expressed in COS-1 cells was about 3% of the wild type.	Irinotecan	27-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
15572581-10	2005	The intrinsic clearance of 7-ethyl-10-hydroxycamptothecin (SN-38) by P229L UGT1A1 expressed in COS-1 cells was about 3% of the wild type.	Irinotecan	59-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
15572581-10	2005	The intrinsic clearance of 7-ethyl-10-hydroxycamptothecin (SN-38) by P229L UGT1A1 expressed in COS-1 cells was about 3% of the wild type.	carbonyl sulfide	95-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
15727486-10	2005	The enzymes responsible for the activation, metabolism and mechanism of action of irinotecan, namely carboxylesterase 2, cytochrome P450 (CYP) 3A4, uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1), and topoisomerase-I, also exhibit variable interindividual activity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-203
15710570-2	2005	We investigated whether susceptibility to cholelithiasis in SCA was associated with the promoter polymorphism of the 5?-diphosphate-glucuronosyltransferase 1A1 (UGT1A1) gene encoding a key enzyme in bilirubin catabolism.	Bilirubin	199-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-167
15557560-1	2005	UDP-glucuronosyltransferase (UGT) 1A1 glucuronidates endogenous metabolites, such as bilirubin, and exogenous substances, and plays a critical role in their detoxification and excretion.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
15557560-2	2005	In a previous article, we described the phenobarbital response activity to a 290-base pair (bp) distal enhancer sequence (-3499/-3210) of the human UGT1A1 gene that is activated by the constitutive androstane receptor (CAR).	Phenobarbital	40-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
15557560-3	2005	Here, we show that dexamethasone at submicromolar concentrations enhances the pregnane X receptor (PXR) activator-mediated expression of the UGT1A1 gene and protein in HepG2 cells.	Dexamethasone	19-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
15727486-10	2005	The enzymes responsible for the activation, metabolism and mechanism of action of irinotecan, namely carboxylesterase 2, cytochrome P450 (CYP) 3A4, uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1), and topoisomerase-I, also exhibit variable interindividual activity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	205-211
15727486-13	2005	CYP3A4 and UGT1A1 activity levels might be predictive of irinotecan toxicity rather than efficacy.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
15881424-1	2005	Crigler-Najjar syndrome type 1 (CN1) is an inherited disorder characterized by the absence of hepatic uridine diphosphoglucuronate glucuronosyltransferase (UDPGT), the enzyme responsible for the conjugation and excretion of bilirubin.	Bilirubin	224-233	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-161
15593333-0	2005	In vitro inhibitory effects of non-steroidal antiinflammatory drugs on UDP-glucuronosyltransferase 1A1-catalysed estradiol 3beta-glucuronidation in human liver microsomes.	Estradiol	113-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-102
15593333-6	2005	The IC50 value of diclofenac for 4-methylumbelliferone glucuronidation in recombinant human UGT1A1 was 57.5 microM, similar to that obtained for E3G using HLM.	Diclofenac	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
15593333-6	2005	The IC50 value of diclofenac for 4-methylumbelliferone glucuronidation in recombinant human UGT1A1 was 57.5 microM, similar to that obtained for E3G using HLM.	Hymecromone	33-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
15593333-7	2005	In conclusion, niflumic acid had the most potent inhibitory effects on UGT1A1-catalysed E3G in HLM among seven NSAID investigated.	Niflumic Acid	15-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
15881424-5	2005	After 2 weeks phenobarbitone was added to promote the enzymatic activity of UDPGT of the transplanted hepatocytes.	Phenobarbital	14-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-81
15720263-8	2005	Uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) genotype has been reported to be associated with time to progression and survival in patients treated with irinotecan.	Irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-55
15720263-8	2005	Uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) genotype has been reported to be associated with time to progression and survival in patients treated with irinotecan.	Irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
16399340-6	2005	In humans, lethal hyperbilirubinemic Crigler-Najjar type 1 and milder diseases/syndromes are due to deleterious to mildly deleterious mutations in the bilirubin-specific UGT1A1 or a common exon.	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
16257834-2	2005	Irinotecan undergoes drug metabolism to form an active SN-38, which is further converted to its beta-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-153
16257834-2	2005	Irinotecan undergoes drug metabolism to form an active SN-38, which is further converted to its beta-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	55-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-153
16257834-2	2005	Irinotecan undergoes drug metabolism to form an active SN-38, which is further converted to its beta-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	beta-glucuronide	96-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-153
16257834-3	2005	A variant in the promoter of UGT1A1 gene, UGT1A1*28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and ADR to irinotecan have been reported.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
16257834-3	2005	A variant in the promoter of UGT1A1 gene, UGT1A1*28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and ADR to irinotecan have been reported.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16257834-4	2005	A case-control study of Japanese cancer patients demonstrated that the patients having UGT1A1*28 were at significantly increased risk of severe ADR to irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
16257834-5	2005	To date, genetic variations of the UGT1A1 gene is the most important hereditary factor to predict severe ADR to irinotecan.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
16257834-7	2005	At present, irinotecan chemotherapy based on a patient"s UGT1A1 genetic status is scientifically reasonable.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
15849716-3	2005	Concentration-dependent changes in UGT1A1 response were evaluated in hepatocyte cultures after treatment with 3-methylchloranthrene, beta-napthoflavone, rifampicin, or phenobarbital.	3-methylchloranthrene	110-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
15849716-3	2005	Concentration-dependent changes in UGT1A1 response were evaluated in hepatocyte cultures after treatment with 3-methylchloranthrene, beta-napthoflavone, rifampicin, or phenobarbital.	beta-napthoflavone	133-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
15849716-3	2005	Concentration-dependent changes in UGT1A1 response were evaluated in hepatocyte cultures after treatment with 3-methylchloranthrene, beta-napthoflavone, rifampicin, or phenobarbital.	Rifampin	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
15849716-3	2005	Concentration-dependent changes in UGT1A1 response were evaluated in hepatocyte cultures after treatment with 3-methylchloranthrene, beta-napthoflavone, rifampicin, or phenobarbital.	Phenobarbital	168-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
15849716-6	2005	Pharmacodynamic modeling revealed EC50 values statistically significant between UGT1A1 and CYP2B6 after treatment with PB, but not statistically distinguishable between UGT1A1 and CYP"s 1A2 or 3A4 after treatment with 3-methylchloranthrene or rifampicin, respectively.	Lead	119-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Rifampin	63-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Ritonavir	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Clotrimazole	90-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Phenobarbital	195-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Phenytoin	213-222	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16399344-8	2005	Similar to regulation of CYP1A1, the transcriptional activation of UGT1A1 by TCDD is mediated through the aryl hydrocarbon receptor.	Polychlorinated Dibenzodioxins	77-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
16399345-1	2005	Human UDP-glucuronosyltransferase (UGT) 1A1 is the enzyme that detoxifies neurotoxic bilirubin by conjugating it with glucuronic acid.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
16399345-1	2005	Human UDP-glucuronosyltransferase (UGT) 1A1 is the enzyme that detoxifies neurotoxic bilirubin by conjugating it with glucuronic acid.	Glucuronic Acid	118-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
16399345-2	2005	In addition to bilirubin, UGT1A1 conjugates various endogenous and exogenous lipophilic compounds such as estrogens and the active metabolite of the anticancer drug irinotecan SN-38.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
16399345-2	2005	In addition to bilirubin, UGT1A1 conjugates various endogenous and exogenous lipophilic compounds such as estrogens and the active metabolite of the anticancer drug irinotecan SN-38.	Irinotecan	176-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
16399345-3	2005	Thus, activation by specific inducers of the UGT1A1 gene is critical in treating patients with unconjugated hyperbili-rubinemia and in preventing side effects of drug treatment such as SN-38-induced toxicity.	Irinotecan	185-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
15965581-1	2005	In bilirubin metabolism, increased destruction of erythrocytes, defect in the function of organic anion transporter polypeptide 2 (OATP2) or UDP-glucuronosyltransferase 1A1 (UGT1A1) may result in unconjugated hyperbilirubinemia.	Bilirubin	3-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-172
15965581-5	2005	The status of the haplotypes of G6PD, OATP2, and UGT1A1 genes affected the odds ratio and the bilirubin levels in the hyperbilirubinemic subjects.	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16399344-5	2005	UDP-glucuronosyltransferase 1A1 (UGT1A1), responsible for the glucuronidation of bilirubin, is controlled in a tissue-specific manner and can be regulated following environmental exposure.	Bilirubin	81-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
16399344-5	2005	UDP-glucuronosyltransferase 1A1 (UGT1A1), responsible for the glucuronidation of bilirubin, is controlled in a tissue-specific manner and can be regulated following environmental exposure.	Bilirubin	81-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
16399344-6	2005	This chapter describes materials and methods for the examination of molecular interactions that control UGT1A1 expression and induction in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Polychlorinated Dibenzodioxins	151-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
16399344-6	2005	This chapter describes materials and methods for the examination of molecular interactions that control UGT1A1 expression and induction in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Polychlorinated Dibenzodioxins	188-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
15378558-1	2004	The effects of beta-estradiol and propofol on human UGT1A1, 1A8 and 1A9 activities were investigated using 4-methylumbelliferone (4-MU) as a substrate for glucuronidation.	Estradiol	15-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
15724447-4	2005	The activities of detoxifying enzymes such as glutathione transferase (GST), quinone reductase (QR) and UDP-glucuronosyl transferase (UDP-GT) were found to be decreased while the hydrogen peroxide level was increased in the lung cancer bearing animals.	Hydrogen Peroxide	179-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
15864124-0	2005	Genetic polymorphism in the phenobarbital-responsive enhancer module of the UDP-glucuronosyltransferase 1A1 gene and irinotecan toxicity.	Phenobarbital	28-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-107
15864124-0	2005	Genetic polymorphism in the phenobarbital-responsive enhancer module of the UDP-glucuronosyltransferase 1A1 gene and irinotecan toxicity.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-107
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	168-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	231-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	231-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
15864124-2	2005	The phenobarbital-responsive enhancer module (PBREM) of the UGT1A1 promoter region has been reportedly associated with the transcriptional activity of the gene.	Phenobarbital	4-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
15864124-12	2005	The determination of T-3279G and UGT1A1*28 genotypes might be clinically useful in predicting severe irinotecan toxicity in cancer patients.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
15684703-2	2004	After delivery of pDNA encoding hUGT1A1 via hepatic vein or femoral artery, in vitro bilirubin glucuronidation activity was detectable in Gunn rat liver and muscle extracts.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-39
15684703-3	2004	Expression of hUGT1A1 in Gunn rat liver or muscle resulted in excretion of bilirubin glucuronides in bile.	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-21
15684703-3	2004	Expression of hUGT1A1 in Gunn rat liver or muscle resulted in excretion of bilirubin glucuronides in bile.	Glucuronides	85-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-21
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-237
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	239-245
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-237
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	239-245
15523087-12	2004	In addition, the presence of a UGT1A1 variant with a (TA)7 repeat in the promoter (UGT1A1*28) was associated with increased exposure to SN-38 (435 ng x h/mL, 95% confidence interval [CI] = 339 to 531 ng x h/mL in patients who are homozygous for wild-type UGT1A1; 631 ng x h/mL, 95% CI = 499 to 762 ng .	Irinotecan	136-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
15523087-12	2004	In addition, the presence of a UGT1A1 variant with a (TA)7 repeat in the promoter (UGT1A1*28) was associated with increased exposure to SN-38 (435 ng x h/mL, 95% confidence interval [CI] = 339 to 531 ng x h/mL in patients who are homozygous for wild-type UGT1A1; 631 ng x h/mL, 95% CI = 499 to 762 ng .	Irinotecan	136-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
15523087-12	2004	In addition, the presence of a UGT1A1 variant with a (TA)7 repeat in the promoter (UGT1A1*28) was associated with increased exposure to SN-38 (435 ng x h/mL, 95% confidence interval [CI] = 339 to 531 ng x h/mL in patients who are homozygous for wild-type UGT1A1; 631 ng x h/mL, 95% CI = 499 to 762 ng .	Irinotecan	136-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
15523087-15	2004	Evaluation of midazolam clearance combined with UGT1A1*28 genotyping may assist with optimization of irinotecan chemotherapy.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
15320866-0	2004	Farnesol is glucuronidated in human liver, kidney and intestine in vitro, and is a novel substrate for UGT2B7 and UGT1A1.	Farnesol	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
15320866-8	2004	Kinetic analysis and inhibition experiments indicate that, in liver microsomes, UGT1A1 is primarily responsible for farnesol glucuronidation; however, in intestine microsomes, UGT2B7 is probably the major isoform involved, with a very-low-micromolar K(m).	Farnesol	116-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
15378558-1	2004	The effects of beta-estradiol and propofol on human UGT1A1, 1A8 and 1A9 activities were investigated using 4-methylumbelliferone (4-MU) as a substrate for glucuronidation.	Propofol	34-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
15378558-1	2004	The effects of beta-estradiol and propofol on human UGT1A1, 1A8 and 1A9 activities were investigated using 4-methylumbelliferone (4-MU) as a substrate for glucuronidation.	Hymecromone	107-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
15378558-2	2004	The formation of 4-MU glucuronide (4-MUG) from 4-MU, in recombinant human UGT 1A1, 1A8 and 1A9 was determined using HPLC with fluorescence detection.	4-methylumbelliferyl glucuronide	17-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-81
15378558-4	2004	beta-estradiol had potent inhibitory effects on UGT1A9 as well as on UGT1A1 with IC(50) values of 2.1 and 7.2 microM, respectively.	Estradiol	0-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
15378558-6	2004	In contrast, beta-estradiol and propofol activated 4-MU glucuronidation in UGT1A1 and 1A8, respectively.	Estradiol	13-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-89
15378558-6	2004	In contrast, beta-estradiol and propofol activated 4-MU glucuronidation in UGT1A1 and 1A8, respectively.	Propofol	32-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-89
15378558-7	2004	This study therefore indicates that the use of beta-estradiol as a specific inhibitor for UGT1A1 should be used with care in the identification of UGT isozymes responsible for glucuronidation in human liver microsomes.	Estradiol	47-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
15688606-3	2004	In particular, uridine diphosphoglucuronosyl transferase 1A1 (UGT1A1) enzyme is responsible for detoxification of irinotecan active metabolite, SN38.	Irinotecan	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
15688606-4	2004	A polymorphic structure in the promoter region (UGT1A1*28) may affect irinotecan toxicity and SN38 plasma level.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
15269186-8	2004	In contrast, tocotrienols induce MDR1 and UGT1A1 but not CYP3A4 expression in intestinal LS180 cells.	Tocotrienols	13-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
15519273-0	2004	Influence of common variants in the pharmacokinetic genes (OATP-C, UGT1A1, and MRP2) on serum bilirubin levels in healthy subjects.	Bilirubin	94-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
15334623-6	2004	Inhibition studies with known inhibitors of UGT (diclofenac, flunitrazepam and bilirubin) confirmed the involvement of UGT1A1, UGT1A3 and UGT2B15 in the formation of 3-hydroxydesloratadine-glucuronide.	3-hydroxydesloratadine-glucuronide	166-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Bilirubin	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
15469406-3	2004	Although multiple genes may play a role in irinotecan activity, the UDP glycuronosyltransferase 1 family, polypeptide A1 (UGT1A1) enzyme has been strongly associated with toxicity.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
15469406-4	2004	A common dinucleotide repeat polymorphism in the UGT1A1 promoter region (UGT1A1*28) has been correlated with severe toxicity in cancer patients receiving irinotecan-containing therapy.	Dinucleoside Phosphates	9-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
15469406-4	2004	A common dinucleotide repeat polymorphism in the UGT1A1 promoter region (UGT1A1*28) has been correlated with severe toxicity in cancer patients receiving irinotecan-containing therapy.	Dinucleoside Phosphates	9-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
15469406-4	2004	A common dinucleotide repeat polymorphism in the UGT1A1 promoter region (UGT1A1*28) has been correlated with severe toxicity in cancer patients receiving irinotecan-containing therapy.	Irinotecan	154-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
15469406-4	2004	A common dinucleotide repeat polymorphism in the UGT1A1 promoter region (UGT1A1*28) has been correlated with severe toxicity in cancer patients receiving irinotecan-containing therapy.	Irinotecan	154-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
15517893-5	2004	RESULTS: Our HPLC assay results showed that both UGT1A1 and UGT1A10 are responsible for SN-38 glucuronidation.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
15517893-6	2004	The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line.	Irinotecan	49-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
15517893-6	2004	The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line.	Irinotecan	56-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	101-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	108-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	140-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	147-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15334623-5	2004	Out of ten recombinant human UDP-glucuronosyltransferases (UGTs), UGT1A1, UGT1A3, UGT1A8 and UGT2B15 exhibited catalytic activity with respect to the formation of 3-hydroxydesloratadine-glucuronide.	3-hydroxydesloratadine-glucuronide	163-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
15334623-6	2004	Inhibition studies with known inhibitors of UGT (diclofenac, flunitrazepam and bilirubin) confirmed the involvement of UGT1A1, UGT1A3 and UGT2B15 in the formation of 3-hydroxydesloratadine-glucuronide.	Bilirubin	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
15334623-7	2004	The results from this study demonstrated that the in vitro formation of 3-hydroxydesloratadine-glucuronide from 3-hydroxydesloratadine was mediated via UGT1A1, UGT1A3 and UGT2B15 in human liver.	3-hydroxydesloratadine-glucuronide	72-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
15334623-7	2004	The results from this study demonstrated that the in vitro formation of 3-hydroxydesloratadine-glucuronide from 3-hydroxydesloratadine was mediated via UGT1A1, UGT1A3 and UGT2B15 in human liver.	3-hydroxydesloratadine	72-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	152-158
15560369-0	2004	Stimulation of transcriptional expression of human UDP-glucuronosyltransferase 1A1 by dexamethasone.	Dexamethasone	86-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-82
15090468-0	2004	Interactions between sulforaphane and apigenin in the induction of UGT1A1 and GSTA1 in CaCo-2 cells.	sulforaphane	21-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
15090468-0	2004	Interactions between sulforaphane and apigenin in the induction of UGT1A1 and GSTA1 in CaCo-2 cells.	Apigenin	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
15090468-3	2004	We show that apigenin induces UGT1A1 transcription (4-fold) but not GSTA1, and that sulforaphane induces both UGT1A1 (3.7-fold) and GSTA1 (2.8-fold) transcription in both dose- and time-dependent manners.	sulforaphane	84-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
15090468-4	2004	The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1 mRNA up to 12-fold, although this interaction was not seen for GSTA1.	sulforaphane	19-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
15090468-4	2004	The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1 mRNA up to 12-fold, although this interaction was not seen for GSTA1.	Apigenin	36-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
15090468-9	2004	Conversely, the induction of UGT1A1 transcription by sulforaphane was totally abolished by PD98059, although PD98059 slightly enhanced (20%) the induction of UGT1A1 by apigenin implying that the induction of UGT1A1 by sulforaphane is mediated by MAPK/extracellular signal-regulated kinase kinase, whereas UGT1A1 induction by apigenin may be associated with NF-kappaB translocation since the NF-kappaB translocation inhibitor, SN50 enhanced the induction of UGT by apigenin.	sulforaphane	53-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
15090468-9	2004	Conversely, the induction of UGT1A1 transcription by sulforaphane was totally abolished by PD98059, although PD98059 slightly enhanced (20%) the induction of UGT1A1 by apigenin implying that the induction of UGT1A1 by sulforaphane is mediated by MAPK/extracellular signal-regulated kinase kinase, whereas UGT1A1 induction by apigenin may be associated with NF-kappaB translocation since the NF-kappaB translocation inhibitor, SN50 enhanced the induction of UGT by apigenin.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	91-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
15090468-9	2004	Conversely, the induction of UGT1A1 transcription by sulforaphane was totally abolished by PD98059, although PD98059 slightly enhanced (20%) the induction of UGT1A1 by apigenin implying that the induction of UGT1A1 by sulforaphane is mediated by MAPK/extracellular signal-regulated kinase kinase, whereas UGT1A1 induction by apigenin may be associated with NF-kappaB translocation since the NF-kappaB translocation inhibitor, SN50 enhanced the induction of UGT by apigenin.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	109-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
15090468-9	2004	Conversely, the induction of UGT1A1 transcription by sulforaphane was totally abolished by PD98059, although PD98059 slightly enhanced (20%) the induction of UGT1A1 by apigenin implying that the induction of UGT1A1 by sulforaphane is mediated by MAPK/extracellular signal-regulated kinase kinase, whereas UGT1A1 induction by apigenin may be associated with NF-kappaB translocation since the NF-kappaB translocation inhibitor, SN50 enhanced the induction of UGT by apigenin.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	109-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
15090468-9	2004	Conversely, the induction of UGT1A1 transcription by sulforaphane was totally abolished by PD98059, although PD98059 slightly enhanced (20%) the induction of UGT1A1 by apigenin implying that the induction of UGT1A1 by sulforaphane is mediated by MAPK/extracellular signal-regulated kinase kinase, whereas UGT1A1 induction by apigenin may be associated with NF-kappaB translocation since the NF-kappaB translocation inhibitor, SN50 enhanced the induction of UGT by apigenin.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	109-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
15090468-9	2004	Conversely, the induction of UGT1A1 transcription by sulforaphane was totally abolished by PD98059, although PD98059 slightly enhanced (20%) the induction of UGT1A1 by apigenin implying that the induction of UGT1A1 by sulforaphane is mediated by MAPK/extracellular signal-regulated kinase kinase, whereas UGT1A1 induction by apigenin may be associated with NF-kappaB translocation since the NF-kappaB translocation inhibitor, SN50 enhanced the induction of UGT by apigenin.	sulforaphane	218-230	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
15090468-10	2004	The results show that UGT1A1 and GSTA1 are regulated by sulforaphane through different signal transduction pathways and the differences in the mechanisms of modulation of UGT1A1 transcription by sulforaphane and apigenin resulted in a synergistic effect between these two compounds in the induction of UGT1A1.	sulforaphane	56-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
15090468-10	2004	The results show that UGT1A1 and GSTA1 are regulated by sulforaphane through different signal transduction pathways and the differences in the mechanisms of modulation of UGT1A1 transcription by sulforaphane and apigenin resulted in a synergistic effect between these two compounds in the induction of UGT1A1.	sulforaphane	56-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
15090468-10	2004	The results show that UGT1A1 and GSTA1 are regulated by sulforaphane through different signal transduction pathways and the differences in the mechanisms of modulation of UGT1A1 transcription by sulforaphane and apigenin resulted in a synergistic effect between these two compounds in the induction of UGT1A1.	sulforaphane	56-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
15090468-10	2004	The results show that UGT1A1 and GSTA1 are regulated by sulforaphane through different signal transduction pathways and the differences in the mechanisms of modulation of UGT1A1 transcription by sulforaphane and apigenin resulted in a synergistic effect between these two compounds in the induction of UGT1A1.	sulforaphane	195-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
15090468-10	2004	The results show that UGT1A1 and GSTA1 are regulated by sulforaphane through different signal transduction pathways and the differences in the mechanisms of modulation of UGT1A1 transcription by sulforaphane and apigenin resulted in a synergistic effect between these two compounds in the induction of UGT1A1.	sulforaphane	195-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
15090468-10	2004	The results show that UGT1A1 and GSTA1 are regulated by sulforaphane through different signal transduction pathways and the differences in the mechanisms of modulation of UGT1A1 transcription by sulforaphane and apigenin resulted in a synergistic effect between these two compounds in the induction of UGT1A1.	sulforaphane	195-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-177
15560369-1	2004	Human UDP-glucuronosyltransferase (UGT) 1A1 is only enzyme in the conjugation of bilirubin for prevention of hyperbilirubinemia and jaundice.	Bilirubin	81-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-43
15560369-10	2004	This region contains HNF1 element, therefore, we speculated that dexamethasone directly and/or indirectly stimulates UGT1A1 expression through this HNF1 region in the promoter region of UGT1A1.	Dexamethasone	65-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
15560369-10	2004	This region contains HNF1 element, therefore, we speculated that dexamethasone directly and/or indirectly stimulates UGT1A1 expression through this HNF1 region in the promoter region of UGT1A1.	Dexamethasone	65-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-192
15560369-11	2004	Thus, we clarified that UGT1A1 was induced by dexamethasone and the key position was the region (-97/-53) in UGT1A1 promoter.	Dexamethasone	46-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
15560369-11	2004	Thus, we clarified that UGT1A1 was induced by dexamethasone and the key position was the region (-97/-53) in UGT1A1 promoter.	Dexamethasone	46-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
15280927-1	2004	SN-38 is the active metabolite of irinotecan and it is metabolised through conjugation by uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
15280927-1	2004	SN-38 is the active metabolite of irinotecan and it is metabolised through conjugation by uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
15280927-2	2004	The major toxicity of irinotecan therapy is diarrhoea, which has been related to the enzymatic activity of UGT1A1.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
15280927-13	2004	The role of the UGT1A1 genotype as a predictor of toxicity in cancer patients receiving irinotecan demands the performance of a randomized trial to ascertain whether genotype-adjusted dosages of the drug can help to establish safe and effective doses not only for patients with the UGT1A1(*)28 homozygous genotype but also for those with the most common UGT1A1 6/6 or 6/7 genotype.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
15357915-8	2004	The most potent inhibition was observed for the reaction between 17alpha-ethynylestradiol and UGT1A1 (K(i) = 10.5 microM), and the weakest interaction was detected for acetaminophen and UGT1A9 (IC(50) &gt; 1 mM).	Ethinyl Estradiol	65-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
15258113-4	2004	Of these UGTs, UGT1A1, 1A9, and 2B7, which are constitutively expressed in human livers, showed remarkable activity toward 8-OH-2,3,7-triCDD.	3,7,8-trichlorooxanthren-2-ol	123-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
15297419-0	2004	Relevance of different UGT1A1 polymorphisms in irinotecan-induced toxicity: a molecular and clinical study of 75 patients.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	306-316	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-95
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	306-316	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-104
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	318-324	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-95
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	318-324	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-104
15310245-0	2004	Human UDP-glucuronosyltransferase 1A1 is the primary enzyme responsible for the N-glucuronidation of N-hydroxy-PhIP in vitro.	Nitrogen	80-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-37
15310245-0	2004	Human UDP-glucuronosyltransferase 1A1 is the primary enzyme responsible for the N-glucuronidation of N-hydroxy-PhIP in vitro.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	101-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-37
15310245-1	2004	UDP-glucuronosyltransferase 1A proteins (UGT1A) catalyze the glucuronidation of many endogenous and xenobiotic compounds including heterocyclic amines and their hydroxylated metabolites.	heterocyclic amines	131-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
15310245-7	2004	UGT1A1 was the most efficient in converting N-hydroxy-PhIP to both conjugates producing five times more of the N(2)-conjugate than UGT1A4, the next most active UGT, and 286 times more than UGT1A7, the least active UGT.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	44-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15310245-7	2004	UGT1A1 was the most efficient in converting N-hydroxy-PhIP to both conjugates producing five times more of the N(2)-conjugate than UGT1A4, the next most active UGT, and 286 times more than UGT1A7, the least active UGT.	Nitrogen	111-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15310245-8	2004	With an apparent K(m) of 52 microM and a K(cat) of 114 min(-)(1), UGT1A1 was also the most catalytically efficient in forming N-hydroxy-PhIP-N(2)-glucuronide.	n-hydroxy-phip-n(2)-glucuronide	126-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
15310245-9	2004	The catalytic efficiency for N-hydroxy-PhIP-N3-glucuronide formation was 8, 10, and 6 times lower for UGT1A1, -1A4, and -1A8, respectively, when compared to the K(cat) values for N-hydroxy-PhIP-N(2)-glucuronide formation.	n-hydroxy-phip-n3-glucuronide	29-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
15310245-9	2004	The catalytic efficiency for N-hydroxy-PhIP-N3-glucuronide formation was 8, 10, and 6 times lower for UGT1A1, -1A4, and -1A8, respectively, when compared to the K(cat) values for N-hydroxy-PhIP-N(2)-glucuronide formation.	n-hydroxy-phip-n(2)-glucuronide	179-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
15310245-10	2004	These results clearly show that UGT1A1 has the highest specificity for glucuronidating N-hydroxy-PhIP.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	87-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
15286088-0	2004	Influence of genetic variants in UGT1A1 and UGT1A9 on the in vivo glucuronidation of SN-38.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
15122071-5	2004	Only minor glucuronidation was observed for thiocoraline by UGT1A1 and UGT1A9 and no glucuronidation was observed in human liver S9 fraction.	thiocoraline	44-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
15286088-1	2004	The uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A9 isoforms are involved in the phase II biotransformation of the irinotecan metabolite, SN-38.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-65
15286088-8	2004	The median AUC ratio of SN-38G to SN-38 was significantly reduced in carriers of the variant UGT1A1(*)28 allele (7.00 [Wt] vs. 6.26 [Het] vs. 2.51 [Var]; p =.022).	Irinotecan	24-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
15286088-1	2004	The uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A9 isoforms are involved in the phase II biotransformation of the irinotecan metabolite, SN-38.	Irinotecan	152-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-65
15286088-8	2004	The median AUC ratio of SN-38G to SN-38 was significantly reduced in carriers of the variant UGT1A1(*)28 allele (7.00 [Wt] vs. 6.26 [Het] vs. 2.51 [Var]; p =.022).	Irinotecan	34-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
15286088-10	2004	Screening for the UGT1A1(*)28 polymorphism may identify patients with altered SN-38 pharmacokinetics.	Irinotecan	78-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
15286088-3	2004	The aim of this study was to evaluate the functional consequence of the UGT1A1(TA)(7)TAA (UGT1A1(*)28), UGT1A9 766G&gt;A (D256N; UGT1A9(*)5), and UGT1A9 98T&gt;C (M33T; UGT1A9(*)3) variants in Caucasian patients treated with irinotecan.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
15099818-0	2004	Bilirubin UDP-glucuronosyltransferase 1A1 (UGT1A1) gene promoter polymorphisms and HPRT, glycophorin A, and micronuclei mutant frequencies in human blood.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-41
15179405-0	2004	UGT1A1 haplotypes associated with reduced glucuronidation and increased serum bilirubin in irinotecan-administered Japanese patients with cancer.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15179405-0	2004	UGT1A1 haplotypes associated with reduced glucuronidation and increased serum bilirubin in irinotecan-administered Japanese patients with cancer.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15179405-10	2004	CONCLUSION: This study identified several UGT1A1 haplotypes significantly associated with the reduced AUC ratio (*28 and *6) and with the increased total bilirubin level (*28, *60, and *IB) and suggested that the novel haplotype *IB might be functionally important.	Bilirubin	154-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
15254716-1	2004	(Uridino-diphosphate)glucuronosyl-transferase enzyme 1A1 isoform (UGT1A1) is involved in glucuronidation of antineoplastic drugs such as SN38, the active metabolite of irinotecan, as well as estrogens and their metabolites.	Irinotecan	168-178	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
15135306-7	2004	Only UGT1A4 catalyzed the N-linked glucuronidation of TAM among recombinant UGTs (UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A9, UGT2B4, UGT2B7, UGT2B15, and UGT2B17) expressed in insect cells.	Tamoxifen	54-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
15155549-10	2004	Silybin was a potent inhibitor of UGT1A1 and was 14- and 20-fold more selective for UGT1A1 than for UGT1A9 and UGT1A6, respectively.	Silybin	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
15155549-10	2004	Silybin was a potent inhibitor of UGT1A1 and was 14- and 20-fold more selective for UGT1A1 than for UGT1A9 and UGT1A6, respectively.	Silybin	0-7	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
15099818-0	2004	Bilirubin UDP-glucuronosyltransferase 1A1 (UGT1A1) gene promoter polymorphisms and HPRT, glycophorin A, and micronuclei mutant frequencies in human blood.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
15099818-1	2004	A dinucleotide repeat polymorphism (5-, 6-, 7-, or 8-TA units) has been identified within the promoter region of UDP-glucuronosyltransferase 1A1 (UGT1A1) gene.	Dinucleoside Phosphates	2-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-144
15099818-1	2004	A dinucleotide repeat polymorphism (5-, 6-, 7-, or 8-TA units) has been identified within the promoter region of UDP-glucuronosyltransferase 1A1 (UGT1A1) gene.	Dinucleoside Phosphates	2-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
15099818-4	2004	Because bilirubin is a known antioxidant, we hypothesized that UGT1A1 repeats associated with higher bilirubin may be protective against oxidative damage.	Bilirubin	8-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
15099818-4	2004	Because bilirubin is a known antioxidant, we hypothesized that UGT1A1 repeats associated with higher bilirubin may be protective against oxidative damage.	Bilirubin	101-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
15007088-0	2004	Genetic variants in the UDP-glucuronosyltransferase 1A1 gene predict the risk of severe neutropenia of irinotecan.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-55
15007088-2	2004	UDP-glucuronosyltransferase 1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38.	Irinotecan	96-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
15007088-2	2004	UDP-glucuronosyltransferase 1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38.	Irinotecan	96-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
15007088-14	2004	CONCLUSION: UGT1A1 genotype and total bilirubin levels are strongly associated with severe neutropenia, and could be used to identify cancer patients predisposed to the severe toxicity of irinotecan.	Irinotecan	188-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
15104253-0	2004	The induction of human UDP-glucuronosyltransferase 1A1 mediated through a distal enhancer module by flavonoids and xenobiotics.	Flavonoids	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-54
15104253-1	2004	We identified the UDP-glucuronosyltransferase (UGT) 1A1 5"-upstream region that confers UGT1A1 induction by various agents, including flavonoids, on a luciferase reporter gene and has the properties of a transcriptional enhancer.	Flavonoids	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-55
15104253-1	2004	We identified the UDP-glucuronosyltransferase (UGT) 1A1 5"-upstream region that confers UGT1A1 induction by various agents, including flavonoids, on a luciferase reporter gene and has the properties of a transcriptional enhancer.	Flavonoids	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15104253-3	2004	Utilizing transactivation experiments with the UGT1A1 290-bp reporter gene, we assessed UGT1A1 induction by various flavonoids.	Flavonoids	116-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15104253-5	2004	The treatment of HepG2 cells with the flavonoids for 24 hr elevated the expression of mRNAs and proteins of UGT1A1 and CYP1A1, while the mRNA levels of CYP2B6, CYP3A4, CAR, PXR and AhR was not altered.	Flavonoids	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
15104253-8	2004	Taken together, the results indicate that UGT1A1 was induced in response to flavonoids and xenobiotics through the transactivation of the 290-bp reporter gene, that was a multi-component enhancer containing CAR, PXR and AhR motifs.	Flavonoids	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
14977865-9	2004	In conclusion, the formation of SCH 60663 is mediated via UGT1A1, UGT1A3, and UGT2B15, and the formation SCH 488128 is mediated via UGT2B7.	SCH 60663	32-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
12969965-1	2004	Etoposide is a substrate for P-glycoprotein, CYP3A4, CYP3A5, and UGT1A1.	Etoposide	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
14977865-7	2004	Recombinant human UGT1A1, UGT1A3, and UGT2B15 all exhibited catalytic activity with respect to the formation of the phenolic glucuronide.	Glucuronides	125-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
14744946-0	2004	Involvement of human hepatic UGT1A1, UGT2B4, and UGT2B7 in the glucuronidation of carvedilol.	Carvedilol	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
14744946-4	2004	The glucuronidation of carvedilol was catalyzed by at least three recombinant UGT isoforms: UGT1A1, UGT2B4, and UGT2B7.	Carvedilol	23-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
14744946-5	2004	UGT2B4 formed both G1 and G2, whereas UGT1A1 and UGT2B7 were responsible for the formation of glucuronide G2 and G1, respectively.	Glucuronides	94-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
14744946-6	2004	The enzyme kinetics for carvedilol glucuronidation by UGT1A1, UGT2B4, and UGT2B7 in addition to human liver microsomes were examined by Lineweaver-Burk analysis.	Carvedilol	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
14978227-1	2004	Human constitutive androstane (or active) receptor (hCAR), a member of the nuclear receptor superfamily NR1I3, regulates the expression of several genes that are mainly involved in the metabolism of endogenous and xenobiotic compounds (e.g., CYP2B6, CYP3A4, and UGT1A1).	androstane	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	262-268
14978227-7	2004	In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter.	Phenobarbital	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
14978227-7	2004	In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter.	Phenobarbital	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
14871858-1	2004	UDP-glucuronosyltransferase (UGT) 1A1 is involved in the inactivation of estradiol (E(2)) and its oxidized metabolites.	Estradiol	73-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
14871858-5	2004	Intrinsic clearances indicated that UGT1A1 had a preference for the glucuronidation of 2-hydroxyestradiol, a metabolite associated with antiproliferative activity.	2-hydroxyestradiol	87-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
14871858-11	2004	These observations suggest that lower expression of UGT1A1 decreases the risk of endometrial cancer by reducing the excretion of 2-hydroxyestradiol, the antiproliferative metabolite of E(2), in the endometrium.	2-hydroxyestradiol	129-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
14871858-11	2004	These observations suggest that lower expression of UGT1A1 decreases the risk of endometrial cancer by reducing the excretion of 2-hydroxyestradiol, the antiproliferative metabolite of E(2), in the endometrium.	Estradiol	185-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
15180166-2	2004	The underlying cause of GS is a polymorphism in the promotor region of the uridine diphosphate glucuronosyltransferase isoform 1A1 gene (UGT1A1*28), its encoded enzyme being responsible for the glucuronidation of bilirubin and presumably acetaminophen.	Bilirubin	213-222	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
15180166-2	2004	The underlying cause of GS is a polymorphism in the promotor region of the uridine diphosphate glucuronosyltransferase isoform 1A1 gene (UGT1A1*28), its encoded enzyme being responsible for the glucuronidation of bilirubin and presumably acetaminophen.	Acetaminophen	238-251	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
15180166-4	2004	Patients with GS might be more susceptible to unexpected side effects while taking acetaminophen and other drugs which are substrates of UGT1A1.	Acetaminophen	83-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
15180166-9	2004	The metabolic ratios unchanged acetaminophen/acetaminophen glucuronide in UGT1A1-wildtypes, heterozygotes and mutants showed no statistically significant differences.	Acetaminophen	31-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
12969965-10	2004	The UGT1A1 6/6 genotype predicted lower catechol AUC.	catechol	40-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
14744740-0	2004	Correlation between the UDP-glucuronosyltransferase (UGT1A1) TATAA box polymorphism and carcinogen detoxification phenotype: significantly decreased glucuronidating activity against benzo(a)pyrene-7,8-dihydrodiol(-) in liver microsomes from subjects with the UGT1A1*28 variant.	benzo	182-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
14744740-0	2004	Correlation between the UDP-glucuronosyltransferase (UGT1A1) TATAA box polymorphism and carcinogen detoxification phenotype: significantly decreased glucuronidating activity against benzo(a)pyrene-7,8-dihydrodiol(-) in liver microsomes from subjects with the UGT1A1*28 variant.	benzo	182-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	259-265
14744740-0	2004	Correlation between the UDP-glucuronosyltransferase (UGT1A1) TATAA box polymorphism and carcinogen detoxification phenotype: significantly decreased glucuronidating activity against benzo(a)pyrene-7,8-dihydrodiol(-) in liver microsomes from subjects with the UGT1A1*28 variant.	pyrene-7,8-dihydrodiol	190-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
14744740-1	2004	Of the hepatic UDP-glucuronosyltransferases (UGTs), only UGT1A1 and UGT1A9 exhibit activity against benzo(a)pyrene-trans-7R,8R-dihydrodiol [BPD(-)], precursor to the highly mutagenic anti-(+)-benzo(a)pyrene-7R,8S-dihydrodiol-9S,10R-epoxide.	-trans-7r,8r-dihydrodiol	114-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
14744740-1	2004	Of the hepatic UDP-glucuronosyltransferases (UGTs), only UGT1A1 and UGT1A9 exhibit activity against benzo(a)pyrene-trans-7R,8R-dihydrodiol [BPD(-)], precursor to the highly mutagenic anti-(+)-benzo(a)pyrene-7R,8S-dihydrodiol-9S,10R-epoxide.	benzo(a)pyrene 7,8-dihydrodiol	140-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
14744740-1	2004	Of the hepatic UDP-glucuronosyltransferases (UGTs), only UGT1A1 and UGT1A9 exhibit activity against benzo(a)pyrene-trans-7R,8R-dihydrodiol [BPD(-)], precursor to the highly mutagenic anti-(+)-benzo(a)pyrene-7R,8S-dihydrodiol-9S,10R-epoxide.	(+)-benzo	188-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
14744740-1	2004	Of the hepatic UDP-glucuronosyltransferases (UGTs), only UGT1A1 and UGT1A9 exhibit activity against benzo(a)pyrene-trans-7R,8R-dihydrodiol [BPD(-)], precursor to the highly mutagenic anti-(+)-benzo(a)pyrene-7R,8S-dihydrodiol-9S,10R-epoxide.	pyrene-7r,8s-dihydrodiol-9s,10r-epoxide	200-239	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
14744740-2	2004	The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)&gt;(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert"s syndrome.	Dinucleoside Phosphates	58-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
14744740-2	2004	The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)&gt;(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert"s syndrome.	Dinucleoside Phosphates	58-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
14744740-2	2004	The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)&gt;(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert"s syndrome.	Dinucleoside Phosphates	58-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
14744740-2	2004	The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)&gt;(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert"s syndrome.	Bilirubin	219-228	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
14744740-2	2004	The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)&gt;(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert"s syndrome.	Bilirubin	219-228	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
14744740-2	2004	The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)&gt;(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert"s syndrome.	Bilirubin	219-228	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
14744740-4	2004	Significant decreases in UGT1A1 protein (P &lt; 0.005) and bilirubin conjugation activity (P &lt; 0.001) were observed in liver microsomes from subjects homozygous for the UGT1A1*28 allelic variant compared with subjects homozygous for the wild-type UGT1A1*1 allele.	Bilirubin	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	172-178
14744740-4	2004	Significant decreases in UGT1A1 protein (P &lt; 0.005) and bilirubin conjugation activity (P &lt; 0.001) were observed in liver microsomes from subjects homozygous for the UGT1A1*28 allelic variant compared with subjects homozygous for the wild-type UGT1A1*1 allele.	Bilirubin	59-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	172-178
14744740-5	2004	Significant decreases in BPD(-) glucuronidation activity (P &lt; 0.02) were observed in subjects with the UGT1A1(*28/*28) genotype compared with subjects having the wild-type UGT1A1(*1/*1) genotype in assays of liver microsomes that included 0.1 mM alpha-naphthylamine, a competitive inhibitor of UGT1A9 and not UGT1A1.	1-Naphthylamine	249-268	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
14744740-8	2004	These data suggest that the UGT1A1 TATAA box polymorphism plays a role in an individual"s overall ability to detoxify benzo(a)pyrene and in cancer risk.	benzo(a)	118-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
14744740-8	2004	These data suggest that the UGT1A1 TATAA box polymorphism plays a role in an individual"s overall ability to detoxify benzo(a)pyrene and in cancer risk.	pyrene	126-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
14633881-0	2003	Haplotype structure of the UDP-glucuronosyltransferase 1A1 (UGT1A1) gene and its relationship to serum total bilirubin concentration in a male Korean population.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-58
12949046-6	2003	In contrast, SFN induced phase II detoxification enzymes, UDP-glucuronosyltransferase 1A1 and glutathione S-transferase A1 mRNA expression.	sulforaphane	13-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-89
14633881-0	2003	Haplotype structure of the UDP-glucuronosyltransferase 1A1 (UGT1A1) gene and its relationship to serum total bilirubin concentration in a male Korean population.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
12914384-8	2003	UGT1A1 (uridine diphoshate-glucuronosyltransferase 1A1) is involved on irinotecan metabolism.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
14586211-0	2003	Weekly regimen of irinotecan/docetaxel in previously treated non-small cell lung cancer patients and correlation with uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism.	Irinotecan	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-165
14586211-0	2003	Weekly regimen of irinotecan/docetaxel in previously treated non-small cell lung cancer patients and correlation with uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism.	Irinotecan	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
14586211-0	2003	Weekly regimen of irinotecan/docetaxel in previously treated non-small cell lung cancer patients and correlation with uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism.	Docetaxel	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
14550264-1	2003	UDP-glucuronosyltransferase form 1A1 (UGT1A1) is the only bilirubin-glucuronidating isoform of this protein, and genetic deficiencies of UGT1A1 cause Crigler-Najjar syndrome, a disorder resulting from nonhemolytic unconjugated hyperbilirubinemia.	Bilirubin	58-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-36
14550264-1	2003	UDP-glucuronosyltransferase form 1A1 (UGT1A1) is the only bilirubin-glucuronidating isoform of this protein, and genetic deficiencies of UGT1A1 cause Crigler-Najjar syndrome, a disorder resulting from nonhemolytic unconjugated hyperbilirubinemia.	Bilirubin	58-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
14550264-1	2003	UDP-glucuronosyltransferase form 1A1 (UGT1A1) is the only bilirubin-glucuronidating isoform of this protein, and genetic deficiencies of UGT1A1 cause Crigler-Najjar syndrome, a disorder resulting from nonhemolytic unconjugated hyperbilirubinemia.	Bilirubin	58-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
14550264-2	2003	Here we have focused on the instability of a translocation-deficient UGT1A1 protein, which has been found in patients with Crigler-Najjar type II, to elucidate the molecular basis underlying the deficiency in glucuronidation of bilirubin.	Bilirubin	228-237	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
14555337-6	2003	Studies aimed at identifying the human liver UDP-glucuronosyltransferase (UGT) enzyme(s) involved in the glucuronidation of bropirimine were carried out using recombinant human UGTs and it was determined that glucuronidation of bropirimine was catalysed by UGT1A1, UGT1A3 and UGT1A9.	bropirimine	124-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	257-263
14555337-12	2003	The results demonstrate that UGT1A9 and to a lesser extent UGT1A1 are responsible for the majority of bropirimine O-glucuronidation in man.	bropirimine	102-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
14705859-2	2003	The orphan nuclear receptor CAR (NR1I3 controls phase I (CYP2B, CYP2C, CYP3A), phase II (UGT1A1), and transporter (SLC21A6, MRP2) genes involved in drug metabolism and bilirubin clearance.	Bilirubin	168-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
12914384-8	2003	UGT1A1 (uridine diphoshate-glucuronosyltransferase 1A1) is involved on irinotecan metabolism.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-54
12730278-3	2003	Although several genetic polymorphisms are reported for UGT1A1 and UGT1A7 that affect the SN-38 glucuronidation activities, no such polymorphisms have been identified for UGT1A9.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
12960109-7	2003	The extent of SN-38 glucuronidation was slightly impaired in homozygous variants of UGT1A1*28, although differences were not statistically significant (P = 0.22).	Irinotecan	14-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
12867491-0	2003	Glucuronidation of HMR1098 in human microsomes: evidence for the involvement of UGT1A1 in the formation of S-glucuronides.	Glucuronides	107-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
12850481-2	2003	The molecular basis of this syndrome usually concerns an additional dinucleotide insertion (TA) in the A(TA)(n)TAA configuration residing in the promoter region of the UGT1 A1 gene.	Dinucleoside Phosphates	68-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	168-175
12850492-1	2003	The promoter region of the UDP glucuronosyltransferase 1 gene (UGT1A1) contains a run of thymine-adenine (TA) repeats, usually six (TA)(6).	thymine-adenine	89-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12850492-1	2003	The promoter region of the UDP glucuronosyltransferase 1 gene (UGT1A1) contains a run of thymine-adenine (TA) repeats, usually six (TA)(6).	Tantalum	106-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12756216-8	2003	The changes in gene expression were also seen in differentiated Caco-2 cells, where sulforaphane was responsible for induction of GSTA1 and quercetin for induction of UGT1A1.	sulforaphane	84-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
12756209-8	2003	Nontraditional kinetics were also observed when other UGT1A1 substrates such as ethinylestradiol, buprenorphine, and anthraflavic acid were studied with both human liver microsomes and recombinant UGT1A1.	2,6-dihydroxyanthraquinone	117-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	197-203
12756216-8	2003	The changes in gene expression were also seen in differentiated Caco-2 cells, where sulforaphane was responsible for induction of GSTA1 and quercetin for induction of UGT1A1.	Quercetin	140-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
12695347-0	2003	Glucuronidation of etoposide in human liver microsomes is specifically catalyzed by UDP-glucuronosyltransferase 1A1.	Etoposide	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-115
12695347-6	2003	The kinetic parameters of etoposide glucuronidation were K(m) = 439.6 +/- 70.7 microM and V(max) = 255.6 +/- 19.2 pmol/min/mg of protein in human liver microsomes and K(m) = 503.2 +/- 110.2 microM and V(max) = was 266.5 +/- 28.6 pmol/min/mg of protein in recombinant UGT1A1.	Etoposide	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	267-273
12695347-7	2003	The etoposide glucuronidation in pooled human liver microsomes was inhibited by bilirubin (IC(50) = 31.7 microM) and estradiol (IC(50) = 34 microM) as typical substrates for UGT1A1.	Bilirubin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
12769780-8	2003	In particular, the UGT1A1*28 allele has been associated with an increased toxicity after irinotecan chemotherapy.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
12695347-11	2003	These results demonstrate that etoposide glucuronidation in human liver microsomes is specifically catalyzed by UGT1A1.	Etoposide	31-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
12800608-0	2003	Irinotecan treatment in cancer patients with UGT1A1 polymorphisms.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
12800608-1	2003	At the present time, pharmacogenetic investigation of irinotecan (CPT-11, Camptosar) therapy is mainly focused on the clinical relevance of genetic variation in the UDP-glucuronosyltransferase (UGT1A1) gene.	Irinotecan	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
12800608-6	2003	Two recent pharmacogenetic trials (one performed in the United States and the other in Japan) investigated the clinical significance of UGT1A1 gene mutations for both the pharmacokinetics of irinotecan metabolites and the toxicity profile.	Irinotecan	191-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
12800608-1	2003	At the present time, pharmacogenetic investigation of irinotecan (CPT-11, Camptosar) therapy is mainly focused on the clinical relevance of genetic variation in the UDP-glucuronosyltransferase (UGT1A1) gene.	Irinotecan	66-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
12800608-1	2003	At the present time, pharmacogenetic investigation of irinotecan (CPT-11, Camptosar) therapy is mainly focused on the clinical relevance of genetic variation in the UDP-glucuronosyltransferase (UGT1A1) gene.	Irinotecan	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
12800608-3	2003	UGT1A1 genotypes associated with Gilbert"s syndrome (a mild intermittent hyperbilirubinemia) are characterized by reduced glucuronidation of SN-38.	Irinotecan	141-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12480553-4	2003	UGT1A1*28 is associated with Gilbert"s syndrome, a deficiency in glucuronidation of bilirubin leading to mild hyperbilirubinemia, whereas UGT1A6*2 may result in low glucuronidation rates of several drugs.	Bilirubin	84-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12435745-3	2003	The activity of recombinant UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT2B4, UGT2B7, and UGT2B15 was almost fully inhibited by 0.2% Triton X-100.	Octoxynol	123-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
12566446-1	2003	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an important physiological role by contributing to the metabolism of endogenous substances such as bilirubin in addition to xenobiotics and drugs.	Bilirubin	146-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
12566446-1	2003	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an important physiological role by contributing to the metabolism of endogenous substances such as bilirubin in addition to xenobiotics and drugs.	Bilirubin	146-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
12566446-3	2003	In this report, we show that in human hepatoma HepG2 cells the UGT1A1 gene is also inducible with aryl hydrocarbon receptor (Ah receptor) ligands such as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene metabolites.	2,3,7,8-tetrachlodibenzo-p-dioxin	154-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12566446-3	2003	In this report, we show that in human hepatoma HepG2 cells the UGT1A1 gene is also inducible with aryl hydrocarbon receptor (Ah receptor) ligands such as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene metabolites.	Polychlorinated Dibenzodioxins	189-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12566446-3	2003	In this report, we show that in human hepatoma HepG2 cells the UGT1A1 gene is also inducible with aryl hydrocarbon receptor (Ah receptor) ligands such as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene metabolites.	beta-Naphthoflavone	196-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12566446-3	2003	In this report, we show that in human hepatoma HepG2 cells the UGT1A1 gene is also inducible with aryl hydrocarbon receptor (Ah receptor) ligands such as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene metabolites.	Benzo(a)pyrene	221-235	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12566446-8	2003	Gel mobility shift analysis confirmed that TCDD induction of nuclear proteins specifically bound to the UGT1A1-XRE, and competition experiments with Ah receptor and Arnt antibodies demonstrated that the nuclear protein was the Ah receptor.	Polychlorinated Dibenzodioxins	43-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
12618960-7	2003	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid and thus enhances bilirubin elimination; therefore, it is an important candidate gene for serum bilirubin.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12618960-7	2003	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid and thus enhances bilirubin elimination; therefore, it is an important candidate gene for serum bilirubin.	Glucuronic Acid	51-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12618960-7	2003	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid and thus enhances bilirubin elimination; therefore, it is an important candidate gene for serum bilirubin.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12618960-7	2003	UGT1A1 catalyzes the conjugation of bilirubin with glucuronic acid and thus enhances bilirubin elimination; therefore, it is an important candidate gene for serum bilirubin.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12618960-10	2003	Our findings suggest that UGT1A1 may be a major gene controlling serum bilirubin levels in the population.	Bilirubin	71-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
12642472-8	2003	Human UGT1A1, 1A8, and 1A9 had high activities with EGCG.	epigallocatechin gallate	52-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
12644700-1	2003	Through a multiplex promoter spanning 218 kb, the phase II UDP-glucuronosyltransferase 1A (UGT1) gene encodes at least eight differently regulated mRNAs whose protein products function as the principal means to eliminate a vast array of steroids, heme metabolites, environmental toxins, and drugs.	Steroids	237-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-89
12644700-1	2003	Through a multiplex promoter spanning 218 kb, the phase II UDP-glucuronosyltransferase 1A (UGT1) gene encodes at least eight differently regulated mRNAs whose protein products function as the principal means to eliminate a vast array of steroids, heme metabolites, environmental toxins, and drugs.	Steroids	237-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-95
12644700-1	2003	Through a multiplex promoter spanning 218 kb, the phase II UDP-glucuronosyltransferase 1A (UGT1) gene encodes at least eight differently regulated mRNAs whose protein products function as the principal means to eliminate a vast array of steroids, heme metabolites, environmental toxins, and drugs.	Heme	247-251	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-89
12644700-1	2003	Through a multiplex promoter spanning 218 kb, the phase II UDP-glucuronosyltransferase 1A (UGT1) gene encodes at least eight differently regulated mRNAs whose protein products function as the principal means to eliminate a vast array of steroids, heme metabolites, environmental toxins, and drugs.	Heme	247-251	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-95
12646172-2	2003	Likewise, bilirubin-UGT1A1 expressed in COS-1 cells was inhibited by curcumin and calphostin-C.	Bilirubin	10-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
12646172-2	2003	Likewise, bilirubin-UGT1A1 expressed in COS-1 cells was inhibited by curcumin and calphostin-C.	Curcumin	69-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
12646172-2	2003	Likewise, bilirubin-UGT1A1 expressed in COS-1 cells was inhibited by curcumin and calphostin-C.	calphostin C	82-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
12646172-4	2003	UGT1A1 incorporated [33P]orthophosphate, which was inhibited by calphostin-C.	Phosphate-33P (9CI)	20-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12646172-4	2003	UGT1A1 incorporated [33P]orthophosphate, which was inhibited by calphostin-C.	Carbon	75-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12570720-6	2003	Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
12570720-6	2003	Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.	Irinotecan	183-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	19-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	95-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	0-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	92-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	7-ethyl-10-hydroxycamptothecin glucuronide	133-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-2	2003	Genetic polymorphisms in UGT1A1 are thought to contribute to severe diarrhea and/or leukopenia caused by CPT-11.	Irinotecan	105-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
12485959-4	2003	However, little information is available on the influence of UGT1A1 polymorphisms in the coding region on the SN-38 glucuronidation activity.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
12485959-5	2003	In the present study, wild-type (WT) and three variant (G71R, P229Q, and Y486D) cDNAs of human UGT1A1s were transiently expressed in COS-1 cells, and the kinetic parameters of these UGT1A1s were determined for SN-38 glucuronidation.	carbonyl sulfide	133-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
12485959-6	2003	A partially reduced UGT1A1 protein expression was observed in COS-1 cells for G71R and Y486D.	carbonyl sulfide	62-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
12485959-7	2003	WT UGT1A1 catalyzed SN-38 glucuronidation with an apparent K(m) value of 11.5 microM, whereas those of G71R, P229Q, and Y486D were 14.0, 18.0, and 63.5 microM, respectively.	Irinotecan	20-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	3-9
12485959-10	2003	The decreased SN-38 glucuronidation efficiency ratio of G71R and P229Q could be critical in combination with other polymorphisms in the UGT1A1 gene.	Irinotecan	14-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
12480553-9	2003	CONCLUSIONS: Most patients with Gilbert"s syndrome, in addition to their reduced B-UGT enzyme activity, may have abnormalities in the glucuronidation of aspirin or coumarin- and dopamine-derivatives, due to this combination of UGT1A1*28 and UGT1A6*2 genotypes.	Aspirin	153-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	227-233
12433820-4	2002	The kinetics of the troglitazone glucuronidation in the recombinant UGT1A10 and UGT1A1 exhibited an atypical pattern of substrate inhibition when the substrate concentration was over 200 micro M. With a Michaelis-Menten equation at 6 to 200 micro M troglitazone, the K(m) value was 11.1 +/- 5.8 micro M and the V(max) value was 33.6 +/- 3.7 pmol/min/mg protein in recombinant UGT1A10.	Troglitazone	20-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
12466075-7	2002	Patients with the UGT1A1 TA*7/TA*7 genotype showed higher mean serum bilirubin levels than did patients who were homozygous for the wild-type allele (Mann-Whitney test 35.5; p &lt; 0.05).	Bilirubin	69-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
12433804-2	2002	Although UGT1A1 uniquely catalyzes the glucuronidation of the endobiotic, bilirubin, and UGT2B7 uniquely catalyzes the glucuronidation of morphine to both the 3-0 glucuronide and the 6-0 glucuronide, both catalyze the glucuronidation of the mixed opioid agonist/antagonist buprenorphine with high efficiency.	Bilirubin	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
12433804-2	2002	Although UGT1A1 uniquely catalyzes the glucuronidation of the endobiotic, bilirubin, and UGT2B7 uniquely catalyzes the glucuronidation of morphine to both the 3-0 glucuronide and the 6-0 glucuronide, both catalyze the glucuronidation of the mixed opioid agonist/antagonist buprenorphine with high efficiency.	Morphine	138-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
12433823-10	2002	In conclusion, the involvement of UGT1A1 and UGT1A9 as well as UGT1A4 in nicotine and cotinine N-glucuronidations in human liver microsomes was suggested, although the contributions of each UGT isoform could not be determined conclusively.	Cotinine	86-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
12433820-4	2002	The kinetics of the troglitazone glucuronidation in the recombinant UGT1A10 and UGT1A1 exhibited an atypical pattern of substrate inhibition when the substrate concentration was over 200 micro M. With a Michaelis-Menten equation at 6 to 200 micro M troglitazone, the K(m) value was 11.1 +/- 5.8 micro M and the V(max) value was 33.6 +/- 3.7 pmol/min/mg protein in recombinant UGT1A10.	Troglitazone	249-261	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
12433823-10	2002	In conclusion, the involvement of UGT1A1 and UGT1A9 as well as UGT1A4 in nicotine and cotinine N-glucuronidations in human liver microsomes was suggested, although the contributions of each UGT isoform could not be determined conclusively.	Nitrogen	95-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
12433820-11	2002	The troglitazone glucuronosyltransferase activity in pooled human liver microsomes was strongly inhibited by bilirubin (IC(50) = 1.9 micro M), a typical substrate of UGT1A1.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
12433804-2	2002	Although UGT1A1 uniquely catalyzes the glucuronidation of the endobiotic, bilirubin, and UGT2B7 uniquely catalyzes the glucuronidation of morphine to both the 3-0 glucuronide and the 6-0 glucuronide, both catalyze the glucuronidation of the mixed opioid agonist/antagonist buprenorphine with high efficiency.	3-0 glucuronide	159-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
12433804-2	2002	Although UGT1A1 uniquely catalyzes the glucuronidation of the endobiotic, bilirubin, and UGT2B7 uniquely catalyzes the glucuronidation of morphine to both the 3-0 glucuronide and the 6-0 glucuronide, both catalyze the glucuronidation of the mixed opioid agonist/antagonist buprenorphine with high efficiency.	6-0 glucuronide	183-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
12433820-12	2002	These results suggested that the troglitazone glucuronidation in human liver would be mainly catalyzed by UGT1A1.	Troglitazone	33-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
12433804-2	2002	Although UGT1A1 uniquely catalyzes the glucuronidation of the endobiotic, bilirubin, and UGT2B7 uniquely catalyzes the glucuronidation of morphine to both the 3-0 glucuronide and the 6-0 glucuronide, both catalyze the glucuronidation of the mixed opioid agonist/antagonist buprenorphine with high efficiency.	Buprenorphine	273-286	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
12433823-7	2002	Nicotine and cotinine N-glucuronidations in pooled human liver microsomes were competitively inhibited by bilirubin as a substrate for UGT1A1 (K(i) = 3.9 and 3.3 micro M), imipramine as a substrate for UGT1A4 (K(i) = 6.1 and 2.7 micro M), and propofol as a substrate for UGT1A9 (K(i) = 6.0 and 12.0 micro M).	Nicotine	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
12433804-5	2002	Etonitazenyl also competitively inhibited the glucuronidation of buprenorphine catalyzed by UGT1A1.	etonitazenyl	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
12433804-5	2002	Etonitazenyl also competitively inhibited the glucuronidation of buprenorphine catalyzed by UGT1A1.	Buprenorphine	65-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
12433823-7	2002	Nicotine and cotinine N-glucuronidations in pooled human liver microsomes were competitively inhibited by bilirubin as a substrate for UGT1A1 (K(i) = 3.9 and 3.3 micro M), imipramine as a substrate for UGT1A4 (K(i) = 6.1 and 2.7 micro M), and propofol as a substrate for UGT1A9 (K(i) = 6.0 and 12.0 micro M).	cotinine n	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
12433804-8	2002	Anthraflavic acid and catechol estrogen glucuronidation, catalyzed by UGT1A1, was also not inhibited by etonitazenyl or buprenorphine.	2,6-dihydroxyanthraquinone	0-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
12433804-8	2002	Anthraflavic acid and catechol estrogen glucuronidation, catalyzed by UGT1A1, was also not inhibited by etonitazenyl or buprenorphine.	catechol	22-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-76
12433823-7	2002	Nicotine and cotinine N-glucuronidations in pooled human liver microsomes were competitively inhibited by bilirubin as a substrate for UGT1A1 (K(i) = 3.9 and 3.3 micro M), imipramine as a substrate for UGT1A4 (K(i) = 6.1 and 2.7 micro M), and propofol as a substrate for UGT1A9 (K(i) = 6.0 and 12.0 micro M).	Bilirubin	106-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
12433823-7	2002	Nicotine and cotinine N-glucuronidations in pooled human liver microsomes were competitively inhibited by bilirubin as a substrate for UGT1A1 (K(i) = 3.9 and 3.3 micro M), imipramine as a substrate for UGT1A4 (K(i) = 6.1 and 2.7 micro M), and propofol as a substrate for UGT1A9 (K(i) = 6.0 and 12.0 micro M).	Propofol	243-251	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
12433823-10	2002	In conclusion, the involvement of UGT1A1 and UGT1A9 as well as UGT1A4 in nicotine and cotinine N-glucuronidations in human liver microsomes was suggested, although the contributions of each UGT isoform could not be determined conclusively.	Nicotine	73-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
12464801-2	2002	UGT1A1 basal transcription is affected by a polymorphic (TA)n repeat, and another important regulatory element is the phenobarbital-responsive enhancer module (PBREM) which might contain variants affecting inducible gene expression.	Phenobarbital	118-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12464801-4	2002	We also investigated the relationship between PBREM-(TA)n haplotypes and the glucuronidation rate of the UGT1A1 substrate SN-38.	Irinotecan	122-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
12386134-0	2002	Differential modulation of UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed estradiol-3-glucuronidation by the addition of UGT1A1 substrates and other compounds to human liver microsomes.	Estradiol	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-58
12386134-0	2002	Differential modulation of UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed estradiol-3-glucuronidation by the addition of UGT1A1 substrates and other compounds to human liver microsomes.	Estradiol	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
12386132-0	2002	Involvement of multiple UDP-glucuronosyltransferase 1A isoforms in glucuronidation of 5-(4"-hydroxyphenyl)-5-phenylhydantoin in human liver microsomes.	hydroxyphenytoin	86-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-54
12386134-0	2002	Differential modulation of UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed estradiol-3-glucuronidation by the addition of UGT1A1 substrates and other compounds to human liver microsomes.	Estradiol	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
12386132-7	2002	The 4"-HPPH O-glucuronidation in pooled human liver microsomes was inhibited by beta-estradiol as a typical substrate for UGT1A1 (IC(50) = 21.1 microM) and imipramine as a typical substrate for UGT1A4 (IC(50) = 57.7 microM).	Estradiol	80-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
12386134-2	2002	In confirmation of previous work using alamethicin-treated HLM pooled from four livers, UGT1A1-catalyzed estradiol-3-glucuronidation demonstrated homotropic activation kinetics (S(50) = 22 microM, Hill coefficient, n = 1.9) whereas estradiol-17-glucuronidation (catalyzed by other UGT enzymes) followed Michaelis-Menten kinetics (K(m) = 7 microM).	Alamethicin	39-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
12386134-2	2002	In confirmation of previous work using alamethicin-treated HLM pooled from four livers, UGT1A1-catalyzed estradiol-3-glucuronidation demonstrated homotropic activation kinetics (S(50) = 22 microM, Hill coefficient, n = 1.9) whereas estradiol-17-glucuronidation (catalyzed by other UGT enzymes) followed Michaelis-Menten kinetics (K(m) = 7 microM).	Estradiol	105-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
12386134-2	2002	In confirmation of previous work using alamethicin-treated HLM pooled from four livers, UGT1A1-catalyzed estradiol-3-glucuronidation demonstrated homotropic activation kinetics (S(50) = 22 microM, Hill coefficient, n = 1.9) whereas estradiol-17-glucuronidation (catalyzed by other UGT enzymes) followed Michaelis-Menten kinetics (K(m) = 7 microM).	Estradiol	232-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
12386134-4	2002	Although the classic UGT1A1 substrate bilirubin was a weak competitive inhibitor of estradiol-3-glucuronidation, the estrogens and anthraflavic acid activated or inhibited estradiol-3-glucuronidation dependent on substrate and effector concentrations.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
12386134-4	2002	Although the classic UGT1A1 substrate bilirubin was a weak competitive inhibitor of estradiol-3-glucuronidation, the estrogens and anthraflavic acid activated or inhibited estradiol-3-glucuronidation dependent on substrate and effector concentrations.	Estradiol	84-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
12351142-7	2002	Glucuronidation of BZ and its analogues exhibited the following relative ranking of UDP-glucuronosyltransferase (UGT) metabolism: UGT1A9&gt;UGT1A4&gt;&gt;UGT2B7&gt;UGT1A6 approximately UGT1A1.	benzidine	19-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
12439224-1	2002	UDP-glucuronosyltransferase 1A1 (UGT1A1) is a polymorphic enzyme responsible for the glucuronidation of structurally diverse drugs, non-drug xenobiotics and endogenous compounds (e.g. bilirubin).	Bilirubin	184-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
12439224-1	2002	UDP-glucuronosyltransferase 1A1 (UGT1A1) is a polymorphic enzyme responsible for the glucuronidation of structurally diverse drugs, non-drug xenobiotics and endogenous compounds (e.g. bilirubin).	Bilirubin	184-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
12439228-2	2002	The mean (SD) value of serum bilirubin in the subjects with G6PD deficiency and homozygous variation in UGT1A1 gene was 51.3 (17.8) micromol/l, which was significantly higher compared to that in the other five subgroups.	Bilirubin	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
12357057-0	2002	Relationship between bilirubin UDP-glucuronosyl transferase 1A1 gene and neonatal hyperbilirubinemia.	Bilirubin	21-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-63
12167566-13	2002	Alpha-DHA-G was formed in incubations of DHA with expressed UGT1A9 (K(m) 32 microM, V(max) 8.9 pmol min(-1) mg(-1)) or UGT2B7 (K(m) 438 microM, V(max) 10.9 pmol mg(-1) min(-1)) but not with UGT1A1 or UGT1A6.	artenimol	6-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
12181437-6	2002	Determination of intrinsic clearances predicts that hepatic UGT1A1 and UGT1A9 and the extrahepatic UGT1A7 are major components in SN-38-G formation, whereas a minor role is suggested for UGT1A6, UGT1A8, and UGT1A10.	Irinotecan	130-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
12167566-13	2002	Alpha-DHA-G was formed in incubations of DHA with expressed UGT1A9 (K(m) 32 microM, V(max) 8.9 pmol min(-1) mg(-1)) or UGT2B7 (K(m) 438 microM, V(max) 10.9 pmol mg(-1) min(-1)) but not with UGT1A1 or UGT1A6.	alpha-dha-g	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
12151360-0	2002	Sulforaphane and its glutathione conjugate but not sulforaphane nitrile induce UDP-glucuronosyl transferase (UGT1A1) and glutathione transferase (GSTA1) in cultured cells.	sulforaphane	0-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
12198827-5	2002	Bilirubin-uridinediphosphate-glucuronosyltransferase (UGT1A1) is the only enzyme involved in the conjugation of bilirubin.	Bilirubin	112-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
12151360-0	2002	Sulforaphane and its glutathione conjugate but not sulforaphane nitrile induce UDP-glucuronosyl transferase (UGT1A1) and glutathione transferase (GSTA1) in cultured cells.	Glutathione	21-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
12151360-2	2002	Using a high-throughput microtitre plate assay and TaqMan real time quantitative RT-PCR to measure mRNA, we show that sulforaphane and its glutathione conjugate, but not the nitrile, increased significantly (P &lt; 0.05) both UGT1A1 and GSTA1 mRNA levels in HepG2 and HT29 cells.	sulforaphane	118-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	226-232
12151360-5	2002	The induction of UGT1A1 and GSTA1 mRNA by sulforaphane was time and concentration dependent.	sulforaphane	42-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
12101428-3	2002	We have constructed a recombinant adenovirus, Ad-hUGT1A1-CTLA4Ig that coexpresses human bilirubin-uridinediphosphoglucuronate glucuronosyltransferase (hUGT1A1) and soluble murine CTLA4Ig, both driven by CMV immediate-early promoters.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-56
12185559-3	2002	Our objective was to investigate whether the UGT2B7 H268Y and UGT1A1*28 polymorphisms contribute to the variability in morphine glucuronide-to-morphine plasma ratios among cancer patients undergoing analgesic therapy with morphine.	Morphine	119-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
12185559-3	2002	Our objective was to investigate whether the UGT2B7 H268Y and UGT1A1*28 polymorphisms contribute to the variability in morphine glucuronide-to-morphine plasma ratios among cancer patients undergoing analgesic therapy with morphine.	Glucuronides	128-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
12101428-3	2002	We have constructed a recombinant adenovirus, Ad-hUGT1A1-CTLA4Ig that coexpresses human bilirubin-uridinediphosphoglucuronate glucuronosyltransferase (hUGT1A1) and soluble murine CTLA4Ig, both driven by CMV immediate-early promoters.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-158
12101428-7	2002	A second injection of Ad-hUGT1A1-CTLA4Ig normalized serum bilirubin.	Bilirubin	58-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-32
12101428-12	2002	In contrast, after Ad-hUGT1A1 (which expresses UGT1A1 alone) injection, serum bilirubin remained normal for only 4 weeks, and returned to preinjection levels by day 120.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-29
12153551-5	2002	In addition, CYP3A and UDPGT are catalysts of many reactions with endobiotics such as steroid hormones.	Steroids	86-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-28
12018987-7	2002	Human UGT1A1, UGT1A8, and UGT1A9 were shown to be especially active in conjugation of both flavonoids, whereas UGT1A4 and UGT1A10 and the isoenzymes from the UGTB family, UGT2B7 and UGT2B15, were less efficient.	Flavonoids	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
12078936-0	2002	Predicting the risk of sporadic elevated bilirubin levels and diagnosing Gilbert"s syndrome by genotyping UGT1A1*28 promoter polymorphism.	Bilirubin	41-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
12078936-3	2002	The aim of this investigation was to evaluate the correlation of unspecific elevated bilirubin levels and the occurrence of GS with a described polymorphism in the uridine diphosphat glucuronosyltransferase 1A1 (UGT1A1) in a predominately Caucasian population.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-210
12078936-3	2002	The aim of this investigation was to evaluate the correlation of unspecific elevated bilirubin levels and the occurrence of GS with a described polymorphism in the uridine diphosphat glucuronosyltransferase 1A1 (UGT1A1) in a predominately Caucasian population.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-218
12078936-10	2002	Genotyping of the UGT1A1 promoter polymorphism is a cheap and unequivocal method for predicting elevated and fluctuating bilirubin levels.	Bilirubin	121-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
12499798-6	2002	METHODS: Promoter regions of the gene for bilirubin UGT-1A1 in twelve patients with Gilbert"s syndrome and twenty healthy subjects (controls) were sequenced.	Bilirubin	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-59
12105841-1	2002	BACKGROUND &amp; AIMS: Coinheritance of the A(TA)7TAA promoter variant in the uridine 5"-diphosphate-glucuronosyl transferase 1A1 (UGT1A1) gene and glucose-6-phosphate dehydrogenase (G6PD) deficiency is crucial to hyperbilirubinemia in white male neonates.	Adenosine Monophosphate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-129
12105841-1	2002	BACKGROUND &amp; AIMS: Coinheritance of the A(TA)7TAA promoter variant in the uridine 5"-diphosphate-glucuronosyl transferase 1A1 (UGT1A1) gene and glucose-6-phosphate dehydrogenase (G6PD) deficiency is crucial to hyperbilirubinemia in white male neonates.	Adenosine Monophosphate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
12051676-6	2002	Catalytic activity of UGT1A01 was determined with 7-hydroxy-4-(trifluoromethyl)-coumarin and more specific human UGT1A1 substrates (1-naphthol, beta-estradiol, 17 alpha-ethinylestradiol, and bilirubin).	1-naphthol	132-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12019197-3	2002	UGT1A1 and 1A8 were found to catalyze the formation of both the 6-beta- and 4"-beta-glucuronides, whereas UGT1A10 formed only the 4"-beta-glucuronide.	6-beta- and 4"-beta-glucuronides	64-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-14
12019197-3	2002	UGT1A1 and 1A8 were found to catalyze the formation of both the 6-beta- and 4"-beta-glucuronides, whereas UGT1A10 formed only the 4"-beta-glucuronide.	4"-beta-glucuronide	76-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-14
12019197-5	2002	Kinetic parameters for raloxifene glucuronidation by expressed UGT1A1 could not be determined due to limited substrate solubility.	Raloxifene Hydrochloride	23-33	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
12023536-8	2002	Among six human UGT isozymes tested, UGT1A1 and 1A3 were capable of catalyzing the glucuronidation of both GFZ and SVA.	Gemfibrozil	107-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-51
12023536-8	2002	Among six human UGT isozymes tested, UGT1A1 and 1A3 were capable of catalyzing the glucuronidation of both GFZ and SVA.	simvastatin hydroxyacid	115-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-51
11950788-0	2002	Induction of human UDP-glucuronosyltransferase UGT1A1 by flavonoids-structural requirements.	Flavonoids	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
11950788-13	2002	Together, these results strongly suggest that the flavonoid induction of UGT1A1 is through a novel nonaryl hydrocarbon receptor-mediated mechanism.	Flavonoids	50-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
11950779-7	2002	Studies with expressed UDP glucuronosyltransferases (UGTs) revealed that both UGT1A1 and UGT1A3 were capable of forming the glucuronide conjugates and the corresponding lactones for all three statins.	Glucuronides	124-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
11950779-7	2002	Studies with expressed UDP glucuronosyltransferases (UGTs) revealed that both UGT1A1 and UGT1A3 were capable of forming the glucuronide conjugates and the corresponding lactones for all three statins.	Lactones	169-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
11950788-1	2002	Recent studies in our laboratory in the human hepatic and intestinal cell lines Hep G2 and Caco-2 have demonstrated induction of UGT1A1 by the flavonoid chrysin (5,7-dihydroxyflavone) using catalytic activity assays and Western and Northern blotting.	Flavonoids	143-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
11950788-1	2002	Recent studies in our laboratory in the human hepatic and intestinal cell lines Hep G2 and Caco-2 have demonstrated induction of UGT1A1 by the flavonoid chrysin (5,7-dihydroxyflavone) using catalytic activity assays and Western and Northern blotting.	chrysin	153-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
11950788-1	2002	Recent studies in our laboratory in the human hepatic and intestinal cell lines Hep G2 and Caco-2 have demonstrated induction of UGT1A1 by the flavonoid chrysin (5,7-dihydroxyflavone) using catalytic activity assays and Western and Northern blotting.	chrysin	162-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	129-135
11950788-2	2002	In the present study, we examined which features of the flavonoid structures were associated with induction of UGT1A1 and whether common drug-metabolizing enzyme inducers also produce this induction.	Flavonoids	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
11990381-0	2002	UGT1A1*28 polymorphism as a determinant of irinotecan disposition and toxicity.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
11983459-0	2002	Crigler-Najjar syndrome type II in a caucasian patient resulting from two mutations in the bilirubin uridine 5"-diphosphate-glucuronosyltransferase (UGT1A1) gene.	Bilirubin	91-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
11956667-1	2002	OBJECTIVE: We investigated how the conserved mutation (Y486D) changed the kinetic parameters of uridine diphosphate glucuronosyltransferase 1A1 and 1A6 (UGT1A1 and 1A6) for 2-amino-5-nitro-4-trifluoromethylphenol, which is a major metabolite of flutamide, a nonsteroidal antiandrogenic agent.	nitro-4-trifluoromethylphenol	183-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-167
11956667-1	2002	OBJECTIVE: We investigated how the conserved mutation (Y486D) changed the kinetic parameters of uridine diphosphate glucuronosyltransferase 1A1 and 1A6 (UGT1A1 and 1A6) for 2-amino-5-nitro-4-trifluoromethylphenol, which is a major metabolite of flutamide, a nonsteroidal antiandrogenic agent.	Flutamide	245-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-167
11956667-5	2002	The Michaelis constant (K(M)) for the aglycone of the wild-type UGT1A1 was double that of the mutant, but the K(M) for UDP-GA of the wild-type UGT1A1 was not significantly different from that of the mutant.	CHEBI:166892	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
11956667-5	2002	The Michaelis constant (K(M)) for the aglycone of the wild-type UGT1A1 was double that of the mutant, but the K(M) for UDP-GA of the wild-type UGT1A1 was not significantly different from that of the mutant.	Uridine Diphosphate	119-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
11956667-5	2002	The Michaelis constant (K(M)) for the aglycone of the wild-type UGT1A1 was double that of the mutant, but the K(M) for UDP-GA of the wild-type UGT1A1 was not significantly different from that of the mutant.	Uridine Diphosphate	119-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	156-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
11990381-4	2002	Here we report the results from a prospective clinical pharmacogenetic study to determine the significance of UGT1A1*28 polymorphism on irinotecan disposition and toxicity in patients with cancer.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11990381-10	2002	The results suggest that screening for UGT1A1*28 polymorphism may identify patients with lower SN-38 glucuronidation rates and greater susceptibility to irinotecan induced gastrointestinal and bone marrow toxicity.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
11990381-10	2002	The results suggest that screening for UGT1A1*28 polymorphism may identify patients with lower SN-38 glucuronidation rates and greater susceptibility to irinotecan induced gastrointestinal and bone marrow toxicity.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
11956667-1	2002	OBJECTIVE: We investigated how the conserved mutation (Y486D) changed the kinetic parameters of uridine diphosphate glucuronosyltransferase 1A1 and 1A6 (UGT1A1 and 1A6) for 2-amino-5-nitro-4-trifluoromethylphenol, which is a major metabolite of flutamide, a nonsteroidal antiandrogenic agent.	Ganciclovir	173-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-167
11915038-0	2002	Hemolysis and bilirubin conjugation in association with UDP-glucuronosyltransferase 1A1 promoter polymorphism.	Bilirubin	14-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
11906189-1	2002	The UDP-glucuronosyltransferase UGT1A1 plays a critical role in the detoxification of potentially neurotoxic bilirubin by conjugating it with glucuronic acid.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
11906189-1	2002	The UDP-glucuronosyltransferase UGT1A1 plays a critical role in the detoxification of potentially neurotoxic bilirubin by conjugating it with glucuronic acid.	Glucuronic Acid	142-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
11906189-2	2002	We identified a polymorphism that results in a T to G substitution at nucleotide number -3263 of the phenobarbital-responsive enhancer module of the UGT1A1 gene, thereby significantly decreasing transcriptional activity as indicated by the luciferase-reporter assay.	Phenobarbital	101-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
11906189-5	2002	Plasma total bilirubin levels in these double heterozygotes were significantly higher than those in control subjects carrying one or other of these mutations singly, indicating that compound heterozygous mutations may result in more strongly reduced UGT1A1 activity.	Bilirubin	13-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	250-256
11805731-4	2002	Interindividual variation of sensitivity to irinotecan is related to large variations of biotransformation of the active metabolite SN-38, some of which would be caused by genetic polymorphism of UGT1A1, an isozyme responsible for the SN-38 glucuronidation.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
11805731-4	2002	Interindividual variation of sensitivity to irinotecan is related to large variations of biotransformation of the active metabolite SN-38, some of which would be caused by genetic polymorphism of UGT1A1, an isozyme responsible for the SN-38 glucuronidation.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
11805731-4	2002	Interindividual variation of sensitivity to irinotecan is related to large variations of biotransformation of the active metabolite SN-38, some of which would be caused by genetic polymorphism of UGT1A1, an isozyme responsible for the SN-38 glucuronidation.	Irinotecan	235-240	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
11805731-9	2002	The 4 subjects carrying UGT1A1*28 allele had values of the AUC(SN-38)/AUC(SN-38G) above the 75th percentile of the total population, suggesting a potential pharmacogenetic/pharmacokinetic relationship.	Irinotecan	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
11805731-9	2002	The 4 subjects carrying UGT1A1*28 allele had values of the AUC(SN-38)/AUC(SN-38G) above the 75th percentile of the total population, suggesting a potential pharmacogenetic/pharmacokinetic relationship.	Irinotecan	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
11848303-8	2002	These results suggest that Kupffer cells play a major role in the mediation of ethanol-stimulated induction of UGT1A1 in liver parenchymal cells.	Ethanol	79-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
11868392-6	2002	UGT1A1 conjugates bilirubin, and mutations of the gene cause hereditary unconjugated hyperbilirubinemias (Crigler-Najjar syndrome and Gilbert"s syndrome).	Bilirubin	18-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	84-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	84-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	156-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
11425418-2	2001	To determine whether this has a genetic basis we compared the bilirubin levels and frequency of gallstones in patients with different alleles of the UGT*1 gene.	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-154
11714888-9	2001	APAP-UGT activities correlated best with propofol-UGT (r = 0.85; UGT1A9) and bilirubin-UGT (r = 0.66; UGT1A1) activities, but poorly with UGT1A6 protein (r = 0.30).	Acetaminophen	0-4	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
11546782-0	2001	Homodimerization of human bilirubin-uridine-diphosphoglucuronate glucuronosyltransferase-1 (UGT1A1) and its functional implications.	Bilirubin	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
11546782-1	2001	Genetic lesions of bilirubin-uridine-diphosphoglucuronate glucuronosyltransferase-1 (UGT1A1) completely or partially abolish hepatic bilirubin glucuronidation, causing Crigler-Najjar syndrome type 1 or 2, respectively.	Bilirubin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
11546782-9	2001	Coexpression of mutagenized and wild-type hUGT1A1 in COS-7 cells showed that the mutant form markedly suppressed the catalytic activity of wild-type hUGT1A1.	carbonyl sulfide	53-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-49
11546782-9	2001	Coexpression of mutagenized and wild-type hUGT1A1 in COS-7 cells showed that the mutant form markedly suppressed the catalytic activity of wild-type hUGT1A1.	carbonyl sulfide	53-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-156
11695848-4	2001	The glucuronidation of SN-38 was catalysed by UGT1A1, UGT1A3, UGT1A6 and UGT1A9 as well as by liver microsomes.	Irinotecan	23-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
11695848-5	2001	Among these UGT isoforms, UGT1A1 showed the highest activity of SN-38 glucuronidation at both low (1 microM) and high (200 microM) substrate concentrations.	Irinotecan	64-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
11695848-10	2001	The UGT isoforms involved in SN-38 glucuronidation could be classified into two types: low-Km types such as UGT1A1 and UGT1A9, and high-Km types such as UGT1A3 and UGT1A6, in terms of affinity toward substrate.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
11695848-14	2001	The activity of SN-38 glucuronidation by liver microsomes and UGT1A1 was effectively inhibited by bilirubin.	Irinotecan	16-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
11695848-14	2001	The activity of SN-38 glucuronidation by liver microsomes and UGT1A1 was effectively inhibited by bilirubin.	Bilirubin	98-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
11556815-9	2001	The bilirubin conjugating UGT1A1 was mainly involved in the 3-O-glucuronidation of trans-resveratrol, whereas the phenol conjugating UGT1A6 activity was restricted to cis-resveratrol.	Bilirubin	4-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
11556815-9	2001	The bilirubin conjugating UGT1A1 was mainly involved in the 3-O-glucuronidation of trans-resveratrol, whereas the phenol conjugating UGT1A6 activity was restricted to cis-resveratrol.	3-o	60-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
11556815-9	2001	The bilirubin conjugating UGT1A1 was mainly involved in the 3-O-glucuronidation of trans-resveratrol, whereas the phenol conjugating UGT1A6 activity was restricted to cis-resveratrol.	Resveratrol	83-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
11556815-9	2001	The bilirubin conjugating UGT1A1 was mainly involved in the 3-O-glucuronidation of trans-resveratrol, whereas the phenol conjugating UGT1A6 activity was restricted to cis-resveratrol.	Resveratrol	167-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
11489791-5	2001	CPT-11 is subject to extensive metabolic conversion by various enzyme systems, including esterases to form SN-38, UGT1A1 mediating glucuronidation of SN-38, as well as CYP3A4, which forms several pharmacologically inactive oxidation products.	Irinotecan	0-6	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
11489791-5	2001	CPT-11 is subject to extensive metabolic conversion by various enzyme systems, including esterases to form SN-38, UGT1A1 mediating glucuronidation of SN-38, as well as CYP3A4, which forms several pharmacologically inactive oxidation products.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
11408353-8	2001	Incubations containing PhIP as substrate formed direct PhIP-glucuronides in microsomes expressing UGT1A1, UGT1A4 and UGT1A9 but at levels averaging 53-fold lower than when N-hydroxy-PhIP was used as the substrate.	phip-glucuronides	55-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
11343231-4	2001	The anti-UGT-positive sera from AIH type 2 patients revealed the strongest immunoreactivity against UGT1A1, the main UGT-isoform involved in the bilirubin glucuronidation.	Bilirubin	145-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
11457662-11	2001	Using microsome preparation (from HK293 cell expressing monkey UGT1A01), the apparent K(m) values were 13, 5 and 6 microM for the conjugation of estradiol, 2-hydroxyestradiol and 2-hydroxyestrone, respectively, and were very similar to the values obtained with human UGT1A1.	Estradiol	145-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	267-273
11457662-11	2001	Using microsome preparation (from HK293 cell expressing monkey UGT1A01), the apparent K(m) values were 13, 5 and 6 microM for the conjugation of estradiol, 2-hydroxyestradiol and 2-hydroxyestrone, respectively, and were very similar to the values obtained with human UGT1A1.	2-hydroxyestradiol	156-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	267-273
11457662-11	2001	Using microsome preparation (from HK293 cell expressing monkey UGT1A01), the apparent K(m) values were 13, 5 and 6 microM for the conjugation of estradiol, 2-hydroxyestradiol and 2-hydroxyestrone, respectively, and were very similar to the values obtained with human UGT1A1.	2-hydroxyestrone	179-195	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	267-273
11343253-0	2001	The phenobarbital response enhancer module in the human bilirubin UDP-glucuronosyltransferase UGT1A1 gene and regulation by the nuclear receptor CAR.	Phenobarbital	4-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
11302935-10	2001	We screened commercially available UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A9, UGT2B7, and UGT2B15 for epirubicin glucuronidation.	Epirubicin	99-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
11343253-1	2001	The UDP-glucuronosyltransferase, UGT1A1, is the critical enzyme responsible for detoxification of the potentially neurotoxic bilirubin by conjugating it with glucuronic acid.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
11343231-8	2001	(2) In vitro immunoinhibition experiments showed that glucuronidation of the anticancer drug flavopiridol by UGT1A1 was more strongly inhibited than its UGT1A9-mediated biotransformation.	alvocidib	93-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
11343253-1	2001	The UDP-glucuronosyltransferase, UGT1A1, is the critical enzyme responsible for detoxification of the potentially neurotoxic bilirubin by conjugating it with glucuronic acid.	Glucuronic Acid	158-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
11259359-7	2001	SN-38, the active metabolite of irinotecan, is glucuronidated to the inactive SN-38 glucuronide by UGT1A1, the isoform catalyzing bilirubin glucuronidation.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
11343253-2	2001	For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver.	Phenobarbital	13-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11343253-2	2001	For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver.	Phenobarbital	28-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11343253-3	2001	We have now delineated the PB response activity to a 290-bp distal enhancer sequence (-3483/-3194) of the UGT1A1 gene.	Phenobarbital	27-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
11259324-5	2001	Chemical inhibition experiments further prove the involvement of UGT1A1 and UGT1A9 in the formation of M1 and M2, as the UGT1A1 substrate bilirubin preferably inhibited M1 over M2 (K(i): 36 and 258 microM, respectively), whereas the UGT1A9 substrate propofol showed a more pronounced decrease in M2 but not in M1 formation (K(i): 47 and 142 microM, respectively).	Bilirubin	138-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
11259359-7	2001	SN-38, the active metabolite of irinotecan, is glucuronidated to the inactive SN-38 glucuronide by UGT1A1, the isoform catalyzing bilirubin glucuronidation.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
11259324-5	2001	Chemical inhibition experiments further prove the involvement of UGT1A1 and UGT1A9 in the formation of M1 and M2, as the UGT1A1 substrate bilirubin preferably inhibited M1 over M2 (K(i): 36 and 258 microM, respectively), whereas the UGT1A9 substrate propofol showed a more pronounced decrease in M2 but not in M1 formation (K(i): 47 and 142 microM, respectively).	Bilirubin	138-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
11259359-7	2001	SN-38, the active metabolite of irinotecan, is glucuronidated to the inactive SN-38 glucuronide by UGT1A1, the isoform catalyzing bilirubin glucuronidation.	7-ethyl-10-hydroxycamptothecin glucuronide	78-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
11259324-5	2001	Chemical inhibition experiments further prove the involvement of UGT1A1 and UGT1A9 in the formation of M1 and M2, as the UGT1A1 substrate bilirubin preferably inhibited M1 over M2 (K(i): 36 and 258 microM, respectively), whereas the UGT1A9 substrate propofol showed a more pronounced decrease in M2 but not in M1 formation (K(i): 47 and 142 microM, respectively).	Propofol	250-258	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
11259359-7	2001	SN-38, the active metabolite of irinotecan, is glucuronidated to the inactive SN-38 glucuronide by UGT1A1, the isoform catalyzing bilirubin glucuronidation.	Bilirubin	130-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
11259359-13	2001	A phenotyping procedure for UGT1A1 has not been identified and genotyping of the UGT1A1 promoter in patients receiving irinotecan may identify patients at increased risk of toxicity.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
11259359-14	2001	A clinical trial at the University of Chicago is ongoing to demonstrate the predictive significance of UGT1A1 genotyping for irinotecan pharmacodynamics.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
11283142-2	2001	It is metabolized to TAS-103-glucuronide (TAS-103-G) predominantly by uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1).	tas-103-glucuronide	21-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-125
11283142-2	2001	It is metabolized to TAS-103-glucuronide (TAS-103-G) predominantly by uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1).	tas-103-glucuronide	21-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
11283142-2	2001	It is metabolized to TAS-103-glucuronide (TAS-103-G) predominantly by uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1).	tas-103-g	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	70-125
11283142-2	2001	It is metabolized to TAS-103-glucuronide (TAS-103-G) predominantly by uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1).	tas-103-g	42-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
11283142-4	2001	In addition, we evaluated the influence of UGT1A1 genotype on the pharmacokinetics and toxicity of TAS-103.	6-((2-(dimethylamino)ethyl)amino)-3-hydroxy-7H-indeno(2,1-c)quinolin-7-one	99-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
11442279-0	2001	Induction of UDP-glucuronosyltransferase UGT1A1 by the flavonoid chrysin in Caco-2 cells--potential role in carcinogen bioinactivation.	Flavonoids	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
11177741-5	2001	Increased toxicity seen in patients treated with CPT-11 may be explained by polymorphism in the UGT1A1 gene, which is responsible for glucuronidation of the active metabolite of CPT-11.	Irinotecan	49-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
11177741-5	2001	Increased toxicity seen in patients treated with CPT-11 may be explained by polymorphism in the UGT1A1 gene, which is responsible for glucuronidation of the active metabolite of CPT-11.	Irinotecan	178-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
11179460-5	2001	Using microsome preparations from human embryonic kidney 293 cells stably expressing each of the 12 human and 11 monkey UGT enzymes cloned to date, the two EM-652-monoglucuronides were detected after incubation with microsomes containing human UGT1A1, UGT1A3, UGT1A8, UGT1A9, and monkey monUGT1A01, monUGT1A03, and monUGT1A09.	em-652-monoglucuronides	156-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	244-250
11230743-0	2001	Hepatic uptake of organic anions affects the plasma bilirubin level in subjects with Gilbert"s syndrome mutations in UGT1A1.	Bilirubin	52-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-123
11230743-1	2001	Although in Gilbert"s syndrome (GS), bilirubin glucuronidation is impaired due to an extra TA in the TATA box of the promoter of the gene for bilirubin UDP-glucuronosyltransferase 1 (UGT1A1), many GS homozygotes lack unconjugated hyperbilirubinemia.	Bilirubin	37-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-189
11230743-8	2001	Within each GS subgroup with defined UGT1A1 mutations, the plasma bilirubin level is in part determined by the organic anion uptake rate, assessed by early plasma disappearance of low-dose BSP.	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11442279-6	2001	RESULTS: Western blot analysis showed that pretreatment of Caco-2 cells with 25 microM chrysin induced UGT1A1 without affecting the expression of UGTs 1A6, 1A9 and 2B7.	chrysin	87-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
11442279-8	2001	Similarly, glucuronidation of quercetin was greatly increased in a UGT1A1-specific way.	Quercetin	30-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
11442279-9	2001	The induction of UGT1A1 in the Caco-2 cells resulted in a 10-fold increase in the glucuronidation of N-hydroxy-PhIP.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	101-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
11442279-10	2001	CONCLUSION: Dietary flavonoid-mediated induction of intestinal UGT1A1 may be important for the glucuronidation and detoxification of colon and other carcinogens as well as for the presystemic metabolism of therapeutic drugs.	Flavonoids	20-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
11783425-0	2001	UGT1A1 polymorphism predicts irinotecan toxicity: evolving proof.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
11159800-4	2001	Intrinsic clearance values for human UGT1A1 and UGT2B7 substrates were an order of magnitude higher in DLM than in HLM (e.g., gemfibrozil: 31 microl/min/mg versus 3.0 microl/min/mg; ketoprofen: 2.4 microl/min/mg versus 0.2 microl/min/mg).	Gemfibrozil	126-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11159800-4	2001	Intrinsic clearance values for human UGT1A1 and UGT2B7 substrates were an order of magnitude higher in DLM than in HLM (e.g., gemfibrozil: 31 microl/min/mg versus 3.0 microl/min/mg; ketoprofen: 2.4 microl/min/mg versus 0.2 microl/min/mg).	Ketoprofen	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11174102-2	2001	Recently, the genetic basis of GS has been identified in caucasian populations : it is related to the insertion of a dinucleotide (TA) in the promoter region of the UGT1A1 gene.	Dinucleoside Phosphates	117-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
11124229-2	2001	Four cloned and expressed human UDP-glucuronosyltransferases (UGT1A1, UGT1A6, UGT1A9, and UGT2B15) were used to screen a series of three potential drug substrates differing only in position of the phenol moiety.	Phenol	197-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
11170257-0	2000	Bilirubin UDP-glucuronosyltransferase 1A1 gene polymorphisms: susceptibility to oxidative damage and cancer?	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-41
11156391-2	2000	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-131
11156391-2	2000	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	41-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-131
11156391-3	2000	Genetic polymorphisms of the UGT1A1 would affect an interindividual variation of the toxicity by irinotecan via the alternation of bioavailability of SN-38.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
11156391-3	2000	Genetic polymorphisms of the UGT1A1 would affect an interindividual variation of the toxicity by irinotecan via the alternation of bioavailability of SN-38.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
11156391-4	2000	In this case-control study, retrospective review of clinical records and determination of UGT1A1 polymorphisms were performed to investigate whether a patient with the variant UGT1A1 genotypes would be at higher risk for severe toxicity by irinotecan.	Irinotecan	240-250	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
11156391-9	2000	Multivariate analysis suggested that the genotype either heterozygous or homozygous for UGT1A1*28 would be a significant risk factor for severe toxicity by irinotecan (P &lt; 0.001; odds ratio, 7.23; 95% confidence interval, 2.52-22.3).	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
11156391-13	2000	We suggest that determination of the UGT1A1 genotypes might be clinically useful for predicting severe toxicity by irinotecan in cancer patients.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11156391-14	2000	This research warrants a prospective trial to corroborate the usefulness of gene diagnosis of UGT1A1 polymorphisms prior tb irinotecan chemotherapy.	Terbium	121-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
11156391-14	2000	This research warrants a prospective trial to corroborate the usefulness of gene diagnosis of UGT1A1 polymorphisms prior tb irinotecan chemotherapy.	Irinotecan	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
11196269-2	2001	We analyzed the association of chemotherapy-induced hyperbilirubinemia with mutations of the bilirubin uridine-5"-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1) from two leukemic patients in whom chemotherapy resulted in a hyperbilirubinemic response.	Bilirubin	57-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
11196269-2	2001	We analyzed the association of chemotherapy-induced hyperbilirubinemia with mutations of the bilirubin uridine-5"-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1) from two leukemic patients in whom chemotherapy resulted in a hyperbilirubinemic response.	Uridine Diphosphate	103-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
11196269-2	2001	We analyzed the association of chemotherapy-induced hyperbilirubinemia with mutations of the bilirubin uridine-5"-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1) from two leukemic patients in whom chemotherapy resulted in a hyperbilirubinemic response.	Uridine Diphosphate	127-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
11201174-1	2000	UDP-glucuronosyltransferases (UGTs) involved in troglitazone glucuronidation in rats and humans have been characterized to support the previous toxicity study on troglitazone in Gunn rats and to examine whether the UGT polymorphism or inhibition of bilirubin metabolism is related to the clinically reported rare cases of liver failure.	Troglitazone	48-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-33
11201174-1	2000	UDP-glucuronosyltransferases (UGTs) involved in troglitazone glucuronidation in rats and humans have been characterized to support the previous toxicity study on troglitazone in Gunn rats and to examine whether the UGT polymorphism or inhibition of bilirubin metabolism is related to the clinically reported rare cases of liver failure.	Troglitazone	162-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-33
11201174-1	2000	UDP-glucuronosyltransferases (UGTs) involved in troglitazone glucuronidation in rats and humans have been characterized to support the previous toxicity study on troglitazone in Gunn rats and to examine whether the UGT polymorphism or inhibition of bilirubin metabolism is related to the clinically reported rare cases of liver failure.	Bilirubin	249-258	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-33
11201174-3	2000	In humans, contribution of UGT1A1 was estimated to be about 30% of the total troglitazone glucuronidation by UGTs, using human liver microsomes and recombinant UGTs.	Troglitazone	77-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
11201174-4	2000	Other UGT1 and UGT2 enzymes seem to be responsible for the rest of the troglitazone glucuronidation in humans.	Troglitazone	71-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-10
11201174-5	2000	The multiplicity of UGTs involved in troglitazone glucuronidation in humans may allow even patients lacking bilirubin UGT (UGT1A1) activity to produce troglitazone glucuronide.	Troglitazone	37-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-23
11201174-5	2000	The multiplicity of UGTs involved in troglitazone glucuronidation in humans may allow even patients lacking bilirubin UGT (UGT1A1) activity to produce troglitazone glucuronide.	Troglitazone	37-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
11201174-5	2000	The multiplicity of UGTs involved in troglitazone glucuronidation in humans may allow even patients lacking bilirubin UGT (UGT1A1) activity to produce troglitazone glucuronide.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-23
11201174-5	2000	The multiplicity of UGTs involved in troglitazone glucuronidation in humans may allow even patients lacking bilirubin UGT (UGT1A1) activity to produce troglitazone glucuronide.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
11201174-5	2000	The multiplicity of UGTs involved in troglitazone glucuronidation in humans may allow even patients lacking bilirubin UGT (UGT1A1) activity to produce troglitazone glucuronide.	TROGLITAZONE GLUCURONIDE	151-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-23
11201174-5	2000	The multiplicity of UGTs involved in troglitazone glucuronidation in humans may allow even patients lacking bilirubin UGT (UGT1A1) activity to produce troglitazone glucuronide.	TROGLITAZONE GLUCURONIDE	151-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
11170257-1	2000	The UDP-glucuronosyltransferase 1A1 (UGT1A1) gene product catalyzes the glucuronidation of serum bilirubin as part of normal heme catabolism.	Bilirubin	97-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-35
11170257-1	2000	The UDP-glucuronosyltransferase 1A1 (UGT1A1) gene product catalyzes the glucuronidation of serum bilirubin as part of normal heme catabolism.	Bilirubin	97-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11170257-1	2000	The UDP-glucuronosyltransferase 1A1 (UGT1A1) gene product catalyzes the glucuronidation of serum bilirubin as part of normal heme catabolism.	Heme	125-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-35
11170257-1	2000	The UDP-glucuronosyltransferase 1A1 (UGT1A1) gene product catalyzes the glucuronidation of serum bilirubin as part of normal heme catabolism.	Heme	125-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11170257-5	2000	We hypothesize that the UGT1A1 TA repeats or other functional polymorphisms resulting in lower serum bilirubin levels may be predictive of genetic susceptibility to oxidative damage and cancer.	Bilirubin	101-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
11038168-6	2000	However, UGT1A1 was the only UGT capable of catalyzing the formation of two glucuronides of the catecholic entacapone.	Glucuronides	76-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
11108431-6	2000	With regard to irinotecan, patients with Gilbert"s syndrome phenotype have reduced inactivation of the active topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38) caused by a mutation in the UDP-glucuronosyltransferase 1A1 gene promoter.	Irinotecan	15-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
11108431-6	2000	With regard to irinotecan, patients with Gilbert"s syndrome phenotype have reduced inactivation of the active topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38) caused by a mutation in the UDP-glucuronosyltransferase 1A1 gene promoter.	Irinotecan	136-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
11108431-6	2000	With regard to irinotecan, patients with Gilbert"s syndrome phenotype have reduced inactivation of the active topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38) caused by a mutation in the UDP-glucuronosyltransferase 1A1 gene promoter.	Irinotecan	168-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
11038168-6	2000	However, UGT1A1 was the only UGT capable of catalyzing the formation of two glucuronides of the catecholic entacapone.	entacapone	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
11013440-0	2000	Genetic lesions of bilirubin uridine-diphosphoglucuronate glucuronosyltransferase (UGT1A1) causing Crigler-Najjar and Gilbert syndromes: correlation of genotype to phenotype.	Bilirubin	19-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
11061796-3	2000	During our study of defects of the bilirubin uridine diphosphate-glucuronosyltransferase gene (UGT1A1) in patients with hereditary unconjugated hyperbilirubinemia (Crigler-Najjar syndrome and Gilbert"s syndrome) and neonatal hyperbilirubinemia, we encountered a prolonged case associated with breastfeeding; after cessation of breastfeeding, the infant"s bilirubin level became normal.	Bilirubin	35-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
11003624-1	2000	Recent research has shown that congenital nonhemolytic low grade hyperbilirubinemias in patients with Gilbert"s syndrome (GS) are linked to mutations in the TATA box upstream of the uridine 5"-diphosphoglucose glucuronosyltransferase (UGT1A1) gene leading to an impaired bilirubin glucuronidation.	Bilirubin	70-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	235-241
11013440-2	2000	Bilirubin-UGT(1) (UGT1A1) is the only isoform that significantly contributes to the conjugation of bilirubin.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
11013440-2	2000	Bilirubin-UGT(1) (UGT1A1) is the only isoform that significantly contributes to the conjugation of bilirubin.	Bilirubin	99-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
11013440-11	2000	Several structural mutations of UGT1A1, for example, a G71R substitution, have been reported to cause mild reduction of UGT activity toward bilirubin, resulting in mild hyperbilirubinemia, consistent with Gilbert syndrome.	Bilirubin	140-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
11097345-4	2000	Polymorphisms in UGT1A1, the major bilirubin-glucuronidating form, often result in a decreased capacity to glucuronidate bilirubin, such as observed in Gilbert Syndrome and some forms of perinatal jaundice.	Bilirubin	35-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
10999728-2	2000	In the liver, SN-38 is glucuronidated (SN-38G) by UGT1A1, which also conjugates bilirubin.	Irinotecan	14-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
11097345-4	2000	Polymorphisms in UGT1A1, the major bilirubin-glucuronidating form, often result in a decreased capacity to glucuronidate bilirubin, such as observed in Gilbert Syndrome and some forms of perinatal jaundice.	Bilirubin	121-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
10999728-2	2000	In the liver, SN-38 is glucuronidated (SN-38G) by UGT1A1, which also conjugates bilirubin.	Irinotecan	39-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
10999728-2	2000	In the liver, SN-38 is glucuronidated (SN-38G) by UGT1A1, which also conjugates bilirubin.	Bilirubin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
11182932-0	2000	Crigler-Najjar syndrome type II resulting from three different mutations in the bilirubin uridine 5"-diphosphate-glucuronosyltransferase (UGT1A1) gene.	Bilirubin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
10950852-0	2000	Induction of UDP-glucuronosyltransferase UGT1A1 by the flavonoid chrysin in the human hepatoma cell line hep G2.	Flavonoids	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
10950852-11	2000	9-fold induction of the glucuronidation of the oral contraceptive drug ethinylestradiol, two of the best known and specific UGT1A1 substrates, demonstrating the potential importance of this induction.	Ethinyl Estradiol	71-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
10975608-1	2000	The activity of uridine-diphosphoglucuronosyl transferase 1 (UGT1) may influence the concentration of serum bilirubin.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-59
10946897-3	2000	The predominant thyroid hormone released from the thyroid gland, T4, and the inactive rT3 are glucuronidated by cloned expressed bilirubin UGT1A1 and also phenol UGT1A9.	Bilirubin	129-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
10975608-1	2000	The activity of uridine-diphosphoglucuronosyl transferase 1 (UGT1) may influence the concentration of serum bilirubin.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-65
10975608-6	2000	Subjects with 6/7 or heterozygous variation within the coding region or compound heterozygous (plus one homozygous) variation had significantly higher bilirubin levels than those with wild UGT1A1 gene.	Bilirubin	151-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
10975608-7	2000	When the 290 subjects were stratified into six groups according to their serum bilirubin concentrations, the bilirubin levels were correlated well to the frequencies of variant UGT1A1 gene.	Bilirubin	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
10975608-7	2000	When the 290 subjects were stratified into six groups according to their serum bilirubin concentrations, the bilirubin levels were correlated well to the frequencies of variant UGT1A1 gene.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
10975608-8	2000	Our results show that there is a strong association between UGT1A1 gene and bilirubin levels in healthy Taiwanese adults.	Bilirubin	76-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
10506112-4	1999	UGT1A1, UGT1A4 and UGT1A9 each metabolized all of the aromatic amines.	aromatic amines	54-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
10821120-7	2000	When a beta-glucuronidase inhibitor such as saccharic acid 1,4-lactone, glycyrrhizin or 1-naphtyl-beta-D-glucuronide was added to the reaction mixture, the bilirubin conjugation activity of the human UGT1A1 was detected.	1-naphtyl-beta-d-glucuronide	88-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	200-206
10821120-7	2000	When a beta-glucuronidase inhibitor such as saccharic acid 1,4-lactone, glycyrrhizin or 1-naphtyl-beta-D-glucuronide was added to the reaction mixture, the bilirubin conjugation activity of the human UGT1A1 was detected.	Bilirubin	156-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	200-206
10821120-8	2000	When geniposide was added to the reaction mixture, the bilirubin conjugation activity of UGT1A1 was not seen.	geniposide	5-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
10821120-8	2000	When geniposide was added to the reaction mixture, the bilirubin conjugation activity of UGT1A1 was not seen.	Bilirubin	55-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
11023036-7	2000	In the ER, bilirubin is conjugated by bilirubin uridine diphosphate (UDP)-glycosyltransferase (bilirubin UGT; UGT1A1) to form mono- and diglucuronides of bilirubin.	mono- and diglucuronides	126-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11023036-7	2000	In the ER, bilirubin is conjugated by bilirubin uridine diphosphate (UDP)-glycosyltransferase (bilirubin UGT; UGT1A1) to form mono- and diglucuronides of bilirubin.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
10850406-1	2000	Gilbert"s syndrome, a genetic deficiency in bilirubin UDP-glucuronosyltransferase (UGT1A1), may dispose to increased toxicity of propafenone in poor metabolizers (PMs) of cytochrome P4502D6 because glucuronidation of propafenone is the major metabolic pathway for drug elimination in PMs.	Propafenone	129-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10850406-1	2000	Gilbert"s syndrome, a genetic deficiency in bilirubin UDP-glucuronosyltransferase (UGT1A1), may dispose to increased toxicity of propafenone in poor metabolizers (PMs) of cytochrome P4502D6 because glucuronidation of propafenone is the major metabolic pathway for drug elimination in PMs.	Propafenone	217-228	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
11023036-7	2000	In the ER, bilirubin is conjugated by bilirubin uridine diphosphate (UDP)-glycosyltransferase (bilirubin UGT; UGT1A1) to form mono- and diglucuronides of bilirubin.	Bilirubin	11-20	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11023036-7	2000	In the ER, bilirubin is conjugated by bilirubin uridine diphosphate (UDP)-glycosyltransferase (bilirubin UGT; UGT1A1) to form mono- and diglucuronides of bilirubin.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
10506112-9	1999	UGT1A1 demonstrated more extensive metabolism of the hydroxamic acid, N-hydroxy-N,N"-diacetylbenzidine, and the ring oxidation product, 3-OH-N,N"-diacetylbenzidine, than it did for the other six amines.	Hydroxamic Acids	53-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
10506112-9	1999	UGT1A1 demonstrated more extensive metabolism of the hydroxamic acid, N-hydroxy-N,N"-diacetylbenzidine, and the ring oxidation product, 3-OH-N,N"-diacetylbenzidine, than it did for the other six amines.	N-hydroxy-N,N'-diacetylbenzidine	70-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
10506112-9	1999	UGT1A1 demonstrated more extensive metabolism of the hydroxamic acid, N-hydroxy-N,N"-diacetylbenzidine, and the ring oxidation product, 3-OH-N,N"-diacetylbenzidine, than it did for the other six amines.	3-oh-n,n"-diacetylbenzidine	136-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
10506112-9	1999	UGT1A1 demonstrated more extensive metabolism of the hydroxamic acid, N-hydroxy-N,N"-diacetylbenzidine, and the ring oxidation product, 3-OH-N,N"-diacetylbenzidine, than it did for the other six amines.	Amines	195-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
10506112-11	1999	The K(m) values for N-acetylbenzidine metabolism by UGT1A1 and UGT1A4 were 0.37 +/- 0.14 and 1.8 +/- 0.4 mM, respectively.	N-acetylbenzidine	20-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
10506112-14	1999	Likewise, the O-glucuronide of 3-OH-benzidine was stable at pH 7.4, with 52% remaining at pH 5.5 after 24 h. These results suggest the following relative ranking of transferase metabolism: UGT1A9 &gt; UGT1A4 &gt; &gt; UGT2B7 &gt; UGT1A6 approximately UGT1A1.	o-glucuronide	14-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
10506112-14	1999	Likewise, the O-glucuronide of 3-OH-benzidine was stable at pH 7.4, with 52% remaining at pH 5.5 after 24 h. These results suggest the following relative ranking of transferase metabolism: UGT1A9 &gt; UGT1A4 &gt; &gt; UGT2B7 &gt; UGT1A6 approximately UGT1A1.	3-oh-benzidine	31-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
10462540-1	1999	UDP-glucuronosyltransferase (UGT) 1A1 (UGT1A1) catalyzes the glucuronidation of bilirubin in liver.	Bilirubin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
10530490-2	1999	Recent molecular genetic studies have determined that the clinical phenotype can be described by a dinucleotide polymorphism in the TATA box promoter of the bilirubin uridine diphosphate-glucuronosyltransferase (UGT-1A1) gene, most frequently (TA)7TAA, affecting up to 36% of Africans, but only 3% of Asians.	Dinucleoside Phosphates	99-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-219
10462540-1	1999	UDP-glucuronosyltransferase (UGT) 1A1 (UGT1A1) catalyzes the glucuronidation of bilirubin in liver.	Bilirubin	80-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
10471066-0	1999	UDP-glucuronosyltransferase (UGT1A1*28 and UGT1A6*2) polymorphisms in Caucasians and Asians: relationships to serum bilirubin concentrations.	Bilirubin	116-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
10421657-5	1999	UGT1A1 protein level correlated strongly with both liver microsomal bilirubin UGT activity and liver UGT1A1 mRNA level (r(2) =.82 and.72, respectively).	Bilirubin	68-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
10421657-8	1999	Hepatocytes isolated from the phenytoin-exposed donors exhibited marked declines in UGT1A1 mRNA levels during culturing.	Phenytoin	30-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
10421657-9	1999	Induction studies using hepatocytes treated for 48 hours with phenobarbital (2 mmol/L), oltipraz (50 micromol/L), or 3-methylcholanthrene (2.5 micromol/L) revealed UGT1A1-inducing effects of phenobarbital, oltipraz, and, in particular, 3-methylcholanthrene.	Methylcholanthrene	117-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
10381366-0	1999	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38) by the human UDP-glucuronosyltransferases encoded at the UGT1 locus.	Irinotecan	19-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-119
10381366-0	1999	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38) by the human UDP-glucuronosyltransferases encoded at the UGT1 locus.	Irinotecan	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-119
10381366-3	1999	In this study, we examined the potential for each of the UGT1-encoded isoforms (UGT1A1 and UGT1A3 through UGT1A10) to glucuronidate SN-38.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-61
10381366-3	1999	In this study, we examined the potential for each of the UGT1-encoded isoforms (UGT1A1 and UGT1A3 through UGT1A10) to glucuronidate SN-38.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
10353933-2	1999	We studied whether the condition was associated with mutations in the gene for bilirubin uridine 5"-diphosphate-glucuronosyltransferase (UGT1A1), a key enzyme of bilirubin catabolism.	Bilirubin	79-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
10353933-2	1999	We studied whether the condition was associated with mutations in the gene for bilirubin uridine 5"-diphosphate-glucuronosyltransferase (UGT1A1), a key enzyme of bilirubin catabolism.	Bilirubin	162-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
10353933-3	1999	DESIGN: We analyzed the UGT1A1 gene in 25 Japanese neonates who had nonphysiologic hyperbilirubinemia (serum bilirubin &gt;257 micromol/L) with no obvious cause.	Bilirubin	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
10353933-7	1999	RESULTS: We found a polymorphism for UGT1A1 in exon 1; a G--&gt;A transition at nucleotide 211 caused arginine to replace glycine at position 71 of corresponding protein product (G71R).	Arginine	102-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
10353933-7	1999	RESULTS: We found a polymorphism for UGT1A1 in exon 1; a G--&gt;A transition at nucleotide 211 caused arginine to replace glycine at position 71 of corresponding protein product (G71R).	Glycine	122-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
10471066-2	1999	Mutations in the promoter of the UGT1A1 gene (UGT1A1*28), resulting in 5, 7 or 8, instead of 6 thymine-adenine (TA) repeats, alter bilirubin conjugation.	thymine-adenine	95-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
10471066-2	1999	Mutations in the promoter of the UGT1A1 gene (UGT1A1*28), resulting in 5, 7 or 8, instead of 6 thymine-adenine (TA) repeats, alter bilirubin conjugation.	thymine-adenine	95-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
10471066-2	1999	Mutations in the promoter of the UGT1A1 gene (UGT1A1*28), resulting in 5, 7 or 8, instead of 6 thymine-adenine (TA) repeats, alter bilirubin conjugation.	Tantalum	112-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
10471066-2	1999	Mutations in the promoter of the UGT1A1 gene (UGT1A1*28), resulting in 5, 7 or 8, instead of 6 thymine-adenine (TA) repeats, alter bilirubin conjugation.	Tantalum	112-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
10471066-2	1999	Mutations in the promoter of the UGT1A1 gene (UGT1A1*28), resulting in 5, 7 or 8, instead of 6 thymine-adenine (TA) repeats, alter bilirubin conjugation.	Bilirubin	131-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
10471066-2	1999	Mutations in the promoter of the UGT1A1 gene (UGT1A1*28), resulting in 5, 7 or 8, instead of 6 thymine-adenine (TA) repeats, alter bilirubin conjugation.	Bilirubin	131-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
10471066-7	1999	Within both ethnic groups, serum bilirubin increased with increased numbers of UGT1A1 promoter TA repeats (P = 0.0001).	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
10471066-8	1999	However, a strong ethnic group-by-UGT1A1 genotype interaction suggests that additional ethnic differences in bilirubin metabolism contribute to observed bilirubin concentrations.	Bilirubin	109-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
10471066-8	1999	However, a strong ethnic group-by-UGT1A1 genotype interaction suggests that additional ethnic differences in bilirubin metabolism contribute to observed bilirubin concentrations.	Bilirubin	153-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
10340924-0	1999	Phenotype-genotype correlation of in vitro SN-38 (active metabolite of irinotecan) and bilirubin glucuronidation in human liver tissue with UGT1A1 promoter polymorphism.	Irinotecan	43-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
10340924-0	1999	Phenotype-genotype correlation of in vitro SN-38 (active metabolite of irinotecan) and bilirubin glucuronidation in human liver tissue with UGT1A1 promoter polymorphism.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
10340924-0	1999	Phenotype-genotype correlation of in vitro SN-38 (active metabolite of irinotecan) and bilirubin glucuronidation in human liver tissue with UGT1A1 promoter polymorphism.	Bilirubin	87-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
10340924-1	1999	BACKGROUND: Hepatic uridine diphosphate glucuronosyltransferase (UGT) isoform 1A1 (UGT1A1) is primarily responsible for the glucuronidation of SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of the anticancer agent irinotecan.	Irinotecan	143-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10340924-1	1999	BACKGROUND: Hepatic uridine diphosphate glucuronosyltransferase (UGT) isoform 1A1 (UGT1A1) is primarily responsible for the glucuronidation of SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of the anticancer agent irinotecan.	Irinotecan	150-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10340924-1	1999	BACKGROUND: Hepatic uridine diphosphate glucuronosyltransferase (UGT) isoform 1A1 (UGT1A1) is primarily responsible for the glucuronidation of SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of the anticancer agent irinotecan.	Irinotecan	229-239	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10340924-2	1999	UGT1A1, also catalyzing the glucuronidation of bilirubin, has been shown to have reduced activity in Gilbert"s syndrome.	Bilirubin	47-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
9848110-3	1998	Three human liver UDP-glucuronosyltransferases, UGT2B7, UGT1A1, and UGT1A3, have been shown to catalyze the glucuronidation of catechol estrogens and lead to their enhanced elimination via urine or bile.	catechol	127-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
10190918-2	1999	The aim of this study was to investigate whether a genetic mutation in the bilirubin UGT1A1 gene, which has been associated with Gilbert"s syndrome in adults, is a contributory factor in prolonged neonatal jaundice.	Bilirubin	75-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
9841869-6	1998	The sudden interruption of maternal glucose supply signals the enhanced expression of UGT1A1, giving a novel explanation for the physiological induction of bilirubin glucuronidation in newborn infants.	Glucose	36-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
9841869-6	1998	The sudden interruption of maternal glucose supply signals the enhanced expression of UGT1A1, giving a novel explanation for the physiological induction of bilirubin glucuronidation in newborn infants.	Bilirubin	156-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
10091405-2	1999	In this paper we tested the hypothesis related to the variability of the glucuronidation bilirubin rate which depends on the configuration of the A(TA)nTAA motif of the UGT1*1 glucuronosyltransferase gene promoter.	Bilirubin	89-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
10091406-3	1999	The presence of seven thymine adenine (TA) repeats reduces the efficiency of transcription of the UGT1A1 gene.	thymine adenine	22-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
10091406-3	1999	The presence of seven thymine adenine (TA) repeats reduces the efficiency of transcription of the UGT1A1 gene.	Tantalum	39-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
10091406-11	1999	This polymorphism, as well as the (TA)7 one, is associated with an increased level of bilirubin and a significant reduction of transcription activity of the UGT1A1 gene.	Bilirubin	86-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
10547036-9	1999	The results indicate that one or more phenol-specific UDP-glucuronosyltransferase 1A isoforms are expressed at above normal levels in this tyrosinemic subject.	Phenol	38-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-84
10547036-9	1999	The results indicate that one or more phenol-specific UDP-glucuronosyltransferase 1A isoforms are expressed at above normal levels in this tyrosinemic subject.	tyrosinemic	139-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-84
9848110-8	1998	Flunitrazepam (FNZ), a competitive inhibitor of morphine glucuronidation in hepatic microsomes, competitively inhibited catechol estrogen glucuronidation catalyzed by UGT2B7(Y), UGT1A1, and UGT1A3.	Flunitrazepam	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	178-184
9848110-8	1998	Flunitrazepam (FNZ), a competitive inhibitor of morphine glucuronidation in hepatic microsomes, competitively inhibited catechol estrogen glucuronidation catalyzed by UGT2B7(Y), UGT1A1, and UGT1A3.	catechol	120-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	178-184
9848110-10	1998	FNZ competitively inhibited buprenorphine glucuronidation with UGT1A1 and UGT2B7 but had no inhibitory activity toward UGT1A3.	Buprenorphine	28-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
9692996-0	1998	Required buried alpha-helical structure in the bilirubin UDP-glucuronosyltransferase, UGT1A1, contains a nonreplaceable phenylalanine.	Phenylalanine	120-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
9692996-1	1998	A conserved hydrophobic region in the bilirubin-type UDP-glucuronosyltransferase isozyme was first uncovered as a consequence of a deleterious mutation in the UGT1A1 (HUG-Br1) isozyme of a Crigler-Najjar (CN) Type I patient.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
9692996-1	1998	A conserved hydrophobic region in the bilirubin-type UDP-glucuronosyltransferase isozyme was first uncovered as a consequence of a deleterious mutation in the UGT1A1 (HUG-Br1) isozyme of a Crigler-Najjar (CN) Type I patient.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-174
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Tyrosine	68-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Tyrosine	68-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	227-233
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Leucine	72-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Leucine	72-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	227-233
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Bilirubin	125-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	227-233
9692996-7	1998	The less hydrophobic buried helix in the phenolic-type UGT1A6 has a Tyr/Leu at position 170/171; this isoform glucuronidated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to that for UGT1A1 of 5.	Bilirubin	182-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
9726089-9	1998	SN-38 is eliminated mainly through conjugation by hepatic uridine glucuronosyltransferase (UGT*1.1), the same isoezyme responsible for glucuronidation of bilirubin.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-98
9789606-0	1998	UGT1A1 genotypes and glucuronidation of SN-38, the active metabolite of irinotecan.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
9789606-1	1998	BACKGROUND: Irinotecan (CPT-11) is metabolized by esterase to form a SN-38, which is further conjugated by UGT1A1.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
9789606-1	1998	BACKGROUND: Irinotecan (CPT-11) is metabolized by esterase to form a SN-38, which is further conjugated by UGT1A1.	Irinotecan	24-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
9789606-1	1998	BACKGROUND: Irinotecan (CPT-11) is metabolized by esterase to form a SN-38, which is further conjugated by UGT1A1.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
9789606-3	1998	We investigated whether there might be an inter-individual difference in pharmacokinetics of SN-38 and its glucuronide, depending on the genotypes of UGT1A1.	Irinotecan	93-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
9726089-9	1998	SN-38 is eliminated mainly through conjugation by hepatic uridine glucuronosyltransferase (UGT*1.1), the same isoezyme responsible for glucuronidation of bilirubin.	Bilirubin	154-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-98
9726089-10	1998	Grade 4 irinotecan-related toxicity (ie, neutropenia, diarrhea) has recently been reported in two patients with deficient UGT*1.1 activity.	Irinotecan	8-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
9497253-2	1998	In all CN-1 patients studied, structural mutations in one of the five exons of the gene (UGT1A1) encoding the uridinediphosphoglucuronate glucuronosyltransferase (UGT) isoform bilirubin-UGT1 were implicated in the absence or inactivation of the enzyme.	Bilirubin	176-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
9639672-7	1998	The UGT1A1*32 protein supported 0-10% normal bilirubin glucuronidation when expressed in COS-1 cells.	Bilirubin	45-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
9639672-8	1998	The I294T coding defect seen at the second allele in SM (CN-II) generated the UGT1A1*33 mutant protein which supported 40-55% normal activity with a normal Km (2.5 microM) for bilirubin.	Bilirubin	176-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
9653159-0	1998	Racial variability in the UDP-glucuronosyltransferase 1 (UGT1A1) promoter: a balanced polymorphism for regulation of bilirubin metabolism?	Bilirubin	117-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
9653159-9	1998	We suggest that the unstable UGT1A1 polymorphism may serve to "fine-tune" the plasma bilirubin level within population groups, maintaining it at a high enough level to provide protection against oxidative damage, but at a level that is sufficiently low to prevent kernicterus in infants.	Bilirubin	85-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
9497253-2	1998	In all CN-1 patients studied, structural mutations in one of the five exons of the gene (UGT1A1) encoding the uridinediphosphoglucuronate glucuronosyltransferase (UGT) isoform bilirubin-UGT1 were implicated in the absence or inactivation of the enzyme.	Bilirubin	176-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-93
9497253-6	1998	Bilirubin-UGT1 mRNA is difficult to obtain, since it is expressed in the liver only.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-14
9466980-8	1998	Gunn rats and CN-I patients lacked SN-38 glucuronidating activity, indicating the role of UGT1 isoform in SN-38 glucuronidation.	Irinotecan	106-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-94
9525311-9	1998	Although the mean level of bilirubin in homozygous Gunn rats 1-2 days after birth was already 14.5-fold higher than that of heterozygous siblings, treatment with Ad5/CMV/hUG-Br1 reduced plasma bilirubin to normal levels within 1 week.	Bilirubin	27-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-177
9525311-9	1998	Although the mean level of bilirubin in homozygous Gunn rats 1-2 days after birth was already 14.5-fold higher than that of heterozygous siblings, treatment with Ad5/CMV/hUG-Br1 reduced plasma bilirubin to normal levels within 1 week.	Bilirubin	193-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-177
9466980-10	1998	Intact SN-38 glucuronidation was observed only in HK293 cells transfected with the UGT1A1 isozyme.	Irinotecan	7-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
9466980-11	1998	These results demonstrate that UGT1A1 is the isoform responsible for SN-38 glucuronidation.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
9466980-12	1998	These findings indicate a genetic predisposition to the metabolism of irinotecan, suggesting that patients with low UGT1A1 activity, such as those with Gilbert"s syndrome, may be at an increased risk for irinotecan toxicity.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
9466980-12	1998	These findings indicate a genetic predisposition to the metabolism of irinotecan, suggesting that patients with low UGT1A1 activity, such as those with Gilbert"s syndrome, may be at an increased risk for irinotecan toxicity.	Irinotecan	204-214	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
9028453-2	1997	This study utilizes this information to identify the bases of deficient bilirubin UDP-glucuronosyltransferase activity encoded by the UGT1A gene for the major bilirubin isozyme, HUG-Br1, in 3 Crigler-Najjar type I individuals and the genotype of an at-risk unborn sibling of one patient.	Bilirubin	72-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	178-185
9224784-4	1997	SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells.	Sodium Dodecyl Sulfate	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
9224784-4	1997	SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells.	11,12-3h	100-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
9224784-4	1997	SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells.	Tretinoin	109-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
9224784-4	1997	SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells.	Tritium	106-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
9224784-4	1997	SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells.	Tretinoin	181-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
9402181-2	1997	Preclinical studies showed that UGT*1.1 is the isozyme responsible for SN-38 glucuronidation.	Irinotecan	71-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-39
9402181-3	1997	Patients with Gilbert"s syndrome have deficient UGT*1.1 activity, therefore may have an increased risk for related CPT-11 toxicity.	Irinotecan	115-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-55
8869742-3	1996	Treatment of humans or hepatoma cell lines with drugs such as phenobarbital causes the induction of hepatic bilirubin UGT by increased transcription from the UGT1 gene.	Phenobarbital	62-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-162
8968658-4	1996	Phenobarbital, phenytoin, primidone and carbamazepine are potent inducers of cytochrome P450 (CYP), epoxide hydrolase and uridine diphosphate glucuronosyltransferase (UDPGT) enzyme systems; oxcarbazepine is a weak inducer of CYP enzymes, probably acting on a few specific isoforms only.	Phenobarbital	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-172
8968658-4	1996	Phenobarbital, phenytoin, primidone and carbamazepine are potent inducers of cytochrome P450 (CYP), epoxide hydrolase and uridine diphosphate glucuronosyltransferase (UDPGT) enzyme systems; oxcarbazepine is a weak inducer of CYP enzymes, probably acting on a few specific isoforms only.	Phenytoin	15-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-172
8968658-4	1996	Phenobarbital, phenytoin, primidone and carbamazepine are potent inducers of cytochrome P450 (CYP), epoxide hydrolase and uridine diphosphate glucuronosyltransferase (UDPGT) enzyme systems; oxcarbazepine is a weak inducer of CYP enzymes, probably acting on a few specific isoforms only.	Primidone	26-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-172
8968658-4	1996	Phenobarbital, phenytoin, primidone and carbamazepine are potent inducers of cytochrome P450 (CYP), epoxide hydrolase and uridine diphosphate glucuronosyltransferase (UDPGT) enzyme systems; oxcarbazepine is a weak inducer of CYP enzymes, probably acting on a few specific isoforms only.	Carbamazepine	40-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-172
8806713-4	1996	The results show that both rat and human UGT1.1 catalyze the glucuronidation of opioids with a relative reactivity of buprenorphine &gt; &gt; nalorphine approximately naltrexone.	Buprenorphine	118-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
8806713-4	1996	The results show that both rat and human UGT1.1 catalyze the glucuronidation of opioids with a relative reactivity of buprenorphine &gt; &gt; nalorphine approximately naltrexone.	Nalorphine	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
8806713-4	1996	The results show that both rat and human UGT1.1 catalyze the glucuronidation of opioids with a relative reactivity of buprenorphine &gt; &gt; nalorphine approximately naltrexone.	Naltrexone	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
8806713-5	1996	Comparison of glucuronidation activities in livers from Crigler-Najjar type 1 patients and normal patients indicates that UGT1.1 catalyzes at least 75% of buprenorphine conjugation in normal human liver.	Buprenorphine	155-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
8806713-7	1996	It was found that both rat and human UGT1.1 exhibited comparable substrate specificities and efficiencies (Vmax/Km) of glucuronide formation for anthraquinones, coumarins, estrogens, flavonoids, and phenolic compounds.	Glucuronides	119-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
8806713-7	1996	It was found that both rat and human UGT1.1 exhibited comparable substrate specificities and efficiencies (Vmax/Km) of glucuronide formation for anthraquinones, coumarins, estrogens, flavonoids, and phenolic compounds.	Anthraquinones	145-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
8806713-7	1996	It was found that both rat and human UGT1.1 exhibited comparable substrate specificities and efficiencies (Vmax/Km) of glucuronide formation for anthraquinones, coumarins, estrogens, flavonoids, and phenolic compounds.	Coumarins	161-170	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
8806713-7	1996	It was found that both rat and human UGT1.1 exhibited comparable substrate specificities and efficiencies (Vmax/Km) of glucuronide formation for anthraquinones, coumarins, estrogens, flavonoids, and phenolic compounds.	Flavonoids	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
8806713-7	1996	It was found that both rat and human UGT1.1 exhibited comparable substrate specificities and efficiencies (Vmax/Km) of glucuronide formation for anthraquinones, coumarins, estrogens, flavonoids, and phenolic compounds.	phenolic compounds	199-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
8619894-4	1996	Recent reports of gut transplantation to reverse the metabolic defect in Gunn rats raised further interest in the expression and distribution of human bilirubin (UDP-GTs (HUG Br 1 and HUG Br 2) in the human alimentary tract.	Bilirubin	151-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	171-192
8869742-3	1996	Treatment of humans or hepatoma cell lines with drugs such as phenobarbital causes the induction of hepatic bilirubin UGT by increased transcription from the UGT1 gene.	Bilirubin	108-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-162
8869742-4	1996	The upstream region of UGT1*1 (bilirubin UGT) was sequenced and found to contain consensus sequences for several transcriptional regulatory elements including a "BARBIE box".	Bilirubin	31-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
8869742-10	1996	The regulation of the biliruibin UGT gene by drugs is not yet understood and it will be important to identify additional genetic elements possibly further than -2kb upstream of the UGT1*1 coding region, which regulate the expression of this gene.	biliruibin	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-187
7852413-8	1995	Recessively inherited mutant alleles for the predominant bilirubin isozyme, the HUG-Br1 protein, substituted Arg for Gly at codon 276 (G276R) in exon 1 of UGT1A abolishing a conserved di-glycine.	Bilirubin	57-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-87
7852413-8	1995	Recessively inherited mutant alleles for the predominant bilirubin isozyme, the HUG-Br1 protein, substituted Arg for Gly at codon 276 (G276R) in exon 1 of UGT1A abolishing a conserved di-glycine.	Glycylglycine	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-87
7852413-9	1995	The mutant HUG-Br1-G276R protein expressed in COS-1 cells had no detectable bilirubin glucuronidating activity at either pH 7.6 or 6.4.	carbonyl sulfide	46-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-18
9224500-5	1995	When jaundice results from inactivation of members of the UGT1 family, conjugation of certain phenols, such as the anesthetic propofol, or synthetic estrogens, such as ethinylestradiol, can also be impaired.	Phenols	94-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-62
9224500-5	1995	When jaundice results from inactivation of members of the UGT1 family, conjugation of certain phenols, such as the anesthetic propofol, or synthetic estrogens, such as ethinylestradiol, can also be impaired.	Propofol	126-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-62
9224500-5	1995	When jaundice results from inactivation of members of the UGT1 family, conjugation of certain phenols, such as the anesthetic propofol, or synthetic estrogens, such as ethinylestradiol, can also be impaired.	Ethinyl Estradiol	168-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-62
1900006-0	1991	Induction of alkoxyresorufin O-dealkylases and UDP-glucuronosyl transferase by phenobarbital and 3-methylcholanthrene in primary cultures of porcine ciliary epithelial cells.	Phenobarbital	79-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-75
7971731-5	1994	Morphine and tricyclic antidepressants are substrates of a liver microsomal uridine diphosphate glucuronyl transferase (UDPGT).	Morphine	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-118
7971731-5	1994	Morphine and tricyclic antidepressants are substrates of a liver microsomal uridine diphosphate glucuronyl transferase (UDPGT).	Morphine	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-125
7971731-7	1994	All drugs inhibited the morphine UDPGT.	Morphine	24-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-38
7971731-9	1994	Lubrol PX activated the morphine-UDPGT four to five times.	Polidocanol	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-38
7971731-9	1994	Lubrol PX activated the morphine-UDPGT four to five times.	Morphine	24-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-38
8226884-8	1993	The code for the predominant bilirubin isozyme, the HUG-Br1 protein, is missing the phenylalanine codon at position 170 in exon 1 of UGT1A, abolishing a conserved diphenylalanine.	Bilirubin	29-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-59
8226884-8	1993	The code for the predominant bilirubin isozyme, the HUG-Br1 protein, is missing the phenylalanine codon at position 170 in exon 1 of UGT1A, abolishing a conserved diphenylalanine.	Phenylalanine	84-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-59
8226884-8	1993	The code for the predominant bilirubin isozyme, the HUG-Br1 protein, is missing the phenylalanine codon at position 170 in exon 1 of UGT1A, abolishing a conserved diphenylalanine.	diphenylalanine	163-178	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-59
8226884-9	1993	We demonstrate that, at the pH (7.6) routinely used for bilirubin glucuronidation studies, both the HUG-Br1 protein and human liver microsomes have approximately one-third the activity seen at the major pH optimum of 6.4 and at low ionic strength.	Bilirubin	56-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-107
8467709-2	1993	The sub-family of UGTs that conjugate bilirubin and phenolic compounds with glucuronic acid has been termed UGT1A1.	Bilirubin	38-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
8467709-2	1993	The sub-family of UGTs that conjugate bilirubin and phenolic compounds with glucuronic acid has been termed UGT1A1.	Glucuronic Acid	76-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
8467709-5	1993	In the present study, we used the cDNA of UGT1A1*4, a bilirubin-conjugating isoform, to localize the UGT1A1 locus in the human genome.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
8467709-5	1993	In the present study, we used the cDNA of UGT1A1*4, a bilirubin-conjugating isoform, to localize the UGT1A1 locus in the human genome.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
1520294-6	1992	In addition, 7,7,7-triphenylheptyl-UDP (0.25-0.50 mM) almost inhibited glucuronidation of 1-naphthol and testosterone catalyzed by the recombinant rat liver UGT-2B1 and human liver UGT-1A1, whose cDNA has been expressed in V79 cells.	7,7,7-Triphenylheptyl UDP	13-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-188
1520294-6	1992	In addition, 7,7,7-triphenylheptyl-UDP (0.25-0.50 mM) almost inhibited glucuronidation of 1-naphthol and testosterone catalyzed by the recombinant rat liver UGT-2B1 and human liver UGT-1A1, whose cDNA has been expressed in V79 cells.	1-naphthol	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-188
1520294-6	1992	In addition, 7,7,7-triphenylheptyl-UDP (0.25-0.50 mM) almost inhibited glucuronidation of 1-naphthol and testosterone catalyzed by the recombinant rat liver UGT-2B1 and human liver UGT-1A1, whose cDNA has been expressed in V79 cells.	Testosterone	105-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	181-188
1900006-0	1991	Induction of alkoxyresorufin O-dealkylases and UDP-glucuronosyl transferase by phenobarbital and 3-methylcholanthrene in primary cultures of porcine ciliary epithelial cells.	Methylcholanthrene	97-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-75
1900006-7	1991	UDP-GT activity increased about 5-fold in PB-treated PE cells and about 4-fold in PB-treated NPE cells in 48 hr.	Phenobarbital	42-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
1900006-7	1991	UDP-GT activity increased about 5-fold in PB-treated PE cells and about 4-fold in PB-treated NPE cells in 48 hr.	Phenobarbital	82-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
1900006-9	1991	Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D.	Phenobarbital	13-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
1900006-9	1991	Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D.	Methylcholanthrene	20-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
1900006-9	1991	Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D.	4-[2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]piperidine-2,6-dione	155-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
1900006-9	1991	Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D.	Dactinomycin	179-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33805415-3	2021	We summarized meta-analyses, genome-wide association studies, clinical trials, drug labels, and guidelines relating to the impact of UGT1A1 polymorphisms on irinotecan, belinostat, pazopanib, or nilotinib toxicities.	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
1898728-1	1991	We report the isolation and characterization of two human liver cDNA clones, HUG-Br1 and HUG-Br2; each encodes a UDP-glucuronosyltransferase enzyme which glucuronidates bilirubin IX alpha to form both the IX alpha C8 and IX alpha C12 monoconjugates and a diconjugate.	Bilirubin	169-178	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-84
33805415-3	2021	We summarized meta-analyses, genome-wide association studies, clinical trials, drug labels, and guidelines relating to the impact of UGT1A1 polymorphisms on irinotecan, belinostat, pazopanib, or nilotinib toxicities.	belinostat	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
33805415-3	2021	We summarized meta-analyses, genome-wide association studies, clinical trials, drug labels, and guidelines relating to the impact of UGT1A1 polymorphisms on irinotecan, belinostat, pazopanib, or nilotinib toxicities.	pazopanib	181-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
33805415-3	2021	We summarized meta-analyses, genome-wide association studies, clinical trials, drug labels, and guidelines relating to the impact of UGT1A1 polymorphisms on irinotecan, belinostat, pazopanib, or nilotinib toxicities.	nilotinib	195-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
33805415-4	2021	For irinotecan, UGT1A1*28 was significantly associated with neutropenia and diarrhea, particularly with doses >= 180 mg/m2, supporting the use of UGT1A1 to guide irinotecan prescribing.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
33805415-4	2021	For irinotecan, UGT1A1*28 was significantly associated with neutropenia and diarrhea, particularly with doses >= 180 mg/m2, supporting the use of UGT1A1 to guide irinotecan prescribing.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
33805415-5	2021	The drug label for belinostat recommends a reduced starting dose of 750 mg/m2 for UGT1A1*28 homozygotes, though published studies supporting this recommendation are sparse.	belinostat	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
33805415-6	2021	There was a correlation between UGT1A1 polymorphisms and pazopanib-induced hepatotoxicity, though further studies are needed to elucidate the role of UGT1A1-guided pazopanib dose adjustments.	pazopanib	57-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
33805415-6	2021	There was a correlation between UGT1A1 polymorphisms and pazopanib-induced hepatotoxicity, though further studies are needed to elucidate the role of UGT1A1-guided pazopanib dose adjustments.	pazopanib	164-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
33232579-0	2021	Drug-drug interaction of atazanavir on UGT1A1-mediated glucuronidation of molidustat in human.	Atazanavir Sulfate	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
33777142-0	2021	UGT1A1 Polymorphism for Irinotecan Dose Escalation in Patients with BRAF-Mutated Metastatic Colorectal Cancer Treated with First-Line Bevacizumab and FOLFIRI.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33777142-0	2021	UGT1A1 Polymorphism for Irinotecan Dose Escalation in Patients with BRAF-Mutated Metastatic Colorectal Cancer Treated with First-Line Bevacizumab and FOLFIRI.	FOLFIRI regimen	150-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33777142-3	2021	In this study, we explored the effects and oncological outcomes of UGT1A1 polymorphism for irinotecan escalation in patients with BRAF-mutated mCRC.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
33762934-0	2021	UGT1A1 rs4148323 A Allele is Associated With Increased 2-Hydroxy Atorvastatin Formation and Higher Death Risk in Chinese Patients With Coronary Artery Disease.	2-hydroxyatorvastatin	55-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33762934-6	2021	The patients carrying A allele for the rs4148323 polymorphism (UGT1A1) showed an increase in 2-hydroxy ATV/ATV ratio (p = 1.69E-07, false discovery rate [FDR] = 8.66E-03) relative to the value in individuals without the variant allele.	Atorvastatin	103-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33762934-6	2021	The patients carrying A allele for the rs4148323 polymorphism (UGT1A1) showed an increase in 2-hydroxy ATV/ATV ratio (p = 1.69E-07, false discovery rate [FDR] = 8.66E-03) relative to the value in individuals without the variant allele.	Atorvastatin	107-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33762934-9	2021	In conclusion, our results suggested that the UGT1A1 rs4148323 A allele was associated with increased 2-hydroxy ATV formation and was a significant death risk factor in Chinese patients with CAD.	Atorvastatin	112-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
33232579-0	2021	Drug-drug interaction of atazanavir on UGT1A1-mediated glucuronidation of molidustat in human.	molidustat	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
33232579-4	2021	Based on preclinical findings, glucuronidation of molidustat was predominantly mediated by the 5"-diphospho-glucuronosyltransferase (UGT) isoform UGT1A1.	molidustat	50-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
33232579-5	2021	Therefore, atazanavir, which is a potent inhibitor of UGT1A1, was chosen for the evaluation of pharmacokinetics and EPO release following a single oral dose of 25 mg molidustat.	Atazanavir Sulfate	11-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
22325916-0	2012	Impact of UGT1A1 gene variants on total bilirubin levels in Gilbert syndrome patients and in healthy subjects.	Bilirubin	40-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
33235483-7	2020	Prevalent UGT1A1 gene [TA]7TAA promoter allelic variant UGT1A1*28, characterized by an extra TA repeat, is associated with low transcriptional and reduced enzymatic effectiveness, decreased SN38 active irinotecan metabolite glucuronidation, vs wild-type UGT1A1*1 [A(TA)6TAA].	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
33235483-7	2020	Prevalent UGT1A1 gene [TA]7TAA promoter allelic variant UGT1A1*28, characterized by an extra TA repeat, is associated with low transcriptional and reduced enzymatic effectiveness, decreased SN38 active irinotecan metabolite glucuronidation, vs wild-type UGT1A1*1 [A(TA)6TAA].	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
33235483-7	2020	Prevalent UGT1A1 gene [TA]7TAA promoter allelic variant UGT1A1*28, characterized by an extra TA repeat, is associated with low transcriptional and reduced enzymatic effectiveness, decreased SN38 active irinotecan metabolite glucuronidation, vs wild-type UGT1A1*1 [A(TA)6TAA].	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
33235483-11	2020	Implementation of up-front evaluation of the five validated DPYD variants and UGT1A1*28 in the multidisciplinary molecular tumor board, also including CRC genetic characterization, addresses potential treatments with fluoropyrimidines and irinotecan associations at proper doses and schedules, particularly for early CRC, MCRC patients fit for intensive regimens or unfit for conventional regimens, requiring treatment modulations, and also for patients who experience severe, unexpected toxicities.	fluoropyrimidines	217-234	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
33235483-11	2020	Implementation of up-front evaluation of the five validated DPYD variants and UGT1A1*28 in the multidisciplinary molecular tumor board, also including CRC genetic characterization, addresses potential treatments with fluoropyrimidines and irinotecan associations at proper doses and schedules, particularly for early CRC, MCRC patients fit for intensive regimens or unfit for conventional regimens, requiring treatment modulations, and also for patients who experience severe, unexpected toxicities.	Irinotecan	239-249	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
32796590-2	2020	Normally, unconjugated bilirubin enters hepatocytes through the uptake transporters organic anion transporting polypeptide (OATP) 1B1 and 1B3, undergoes glucuronidation by the Phase II enzyme UDP glucuronosyltransferase 1A1 (UGT1A1), and conjugated forms are excreted into the bile by the canalicular export pump multidrug resistance protein 2 (MRP2).	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-223
32796590-2	2020	Normally, unconjugated bilirubin enters hepatocytes through the uptake transporters organic anion transporting polypeptide (OATP) 1B1 and 1B3, undergoes glucuronidation by the Phase II enzyme UDP glucuronosyltransferase 1A1 (UGT1A1), and conjugated forms are excreted into the bile by the canalicular export pump multidrug resistance protein 2 (MRP2).	Bilirubin	23-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	225-231
22325916-2	2012	This work investigated the effect of UGT1A1 variants on total bilirubin levels in Gilbert patients (n=45) and healthy controls (n=161).	Bilirubin	62-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
22325916-12	2012	Alterations in the UGT1A1 coding region seem to be associated with increased bilirubin levels, and, therefore, with Gilbert syndrome.	Bilirubin	77-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
34734679-6	2022	Genotypes NR1I2 rs2472677 C>T, NR1I2 rs6785049 G>A, SLCO1B1 rs4363657 T>C, SLCO1A2 rs4762699 T>C, and UGT1A1 rs4148323 G>A contributed to individual variation in rocuronium.	Rocuronium	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
34910929-8	2022	For UGT, negligible to moderate inhibition by vicagrel was observed with IC50 values of >50.0, >50.0, 28.2, 8.7, >50.0 and 28.2 muM for UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A9 and UGT2B7, respectively.	methyl 2-(2-acetoxy-6,7-dihydrothieno(3,2-c)pyridin-5(4H)-yl)-2-(2-chlorophenyl)acetate	46-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
34734679-9	2022	Genetic variations in NR1I2 rs2472677, NR1I2 rs6785049, SLCO1B1 rs4363657, SLCO1A2 rs4762699, and UGT1A1 rs4148323 were related to extensive interindividual variability in the clinical duration and total clinical action time of rocuronium.	Rocuronium	228-238	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
34625956-5	2022	We used a common variant in UGT1A1 (rs6742078) associated with an 26% increase in bilirubin levels in the genetic studies.	Bilirubin	82-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
34888851-4	2022	Letermovir is a substrate of UGT1A1/3, P-gp, and OATP1B, with its clearance primarily mediated by OATP1B.	letermovir	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-37
34931017-4	2021	The most active compound 6, a lathyrane diterpenoid (5/11/3 ring system), dose-dependently activated hPXR with a high selectivity, and significantly upregulated the expression of hPXR downstream genes CYP3A4 and UGT1A1.	lathyrane diterpenoid	30-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	212-218
34943103-2	2021	The aim of our study was to assess the role of bilirubin, and the heme oxygenase 1 (HMOX1) and bilirubin UDP-glucuronosyl transferase (UGT1A1) promoter gene variants, which are involved in bilirubin homeostasis, in the NAFLD development in adult patients.	Bilirubin	95-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
34943103-2	2021	The aim of our study was to assess the role of bilirubin, and the heme oxygenase 1 (HMOX1) and bilirubin UDP-glucuronosyl transferase (UGT1A1) promoter gene variants, which are involved in bilirubin homeostasis, in the NAFLD development in adult patients.	Bilirubin	189-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
34943103-5	2021	The (GT)n/(TA)n dinucleotide variations in HMOX1/UGT1A1 gene promoters, respectively, were analyzed by fragment analysis.	Nitrogen	8-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
34943103-5	2021	The (GT)n/(TA)n dinucleotide variations in HMOX1/UGT1A1 gene promoters, respectively, were analyzed by fragment analysis.	(ta)n dinucleotide	10-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
34697081-7	2022	When exposed to a low dose of CPT-11 (10 mg/kg), hUGT1A1HEP mice displayed greater intestinal inflammatory (IL-1beta and IL-6) insult in addition to p53-triggered apoptotic responses.	Irinotecan	30-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-56
34697081-9	2022	When we examined the induction of ER stress in organoids with thapsigargin (TGN), an inhibitor of sarco/endoplasmic reticulum Ca2+ ATPase (SERCA), apoptosis and the caspase surge that occurred in hUGT1A1HEP mice were blocked in hUGT1A1GI organoids.	Thapsigargin	62-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-203
34895177-2	2021	OBJECTIVE: To investigate the association between neonatal hyperbilirubinemia and co-inheritance of G6PD deficiency and 211 G to A variation of UGT1A1 in Chaozhou city of eastern Guangdong province, the effects of G6PD deficiency and UGT1A1 gene variant on the bilirubin level were determined in neonates with hyperbilirubinemia.	Bilirubin	261-270	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
34895177-2	2021	OBJECTIVE: To investigate the association between neonatal hyperbilirubinemia and co-inheritance of G6PD deficiency and 211 G to A variation of UGT1A1 in Chaozhou city of eastern Guangdong province, the effects of G6PD deficiency and UGT1A1 gene variant on the bilirubin level were determined in neonates with hyperbilirubinemia.	Bilirubin	261-270	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	234-240
34847314-4	2021	Additional, well-planned trials of the UGT1A1 genotype-based approach to irinotecan therapy are predicted to reduce adverse drug events in people with the UGT1A1*28/*28 genotypes and improve treatment efficacy in the rest of the patients, which might be cost-effective.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
34478607-7	2021	Inhibition kinetic analyses demonstrated that MOA competitively inhibited UGT1A1-catalyzed NHPH-O-glucuronidation in both hUGT1A1 and HLM, with Ki values of 0.52 muM and 1.22 muM, respectively.	nhph-o	91-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
34478607-7	2021	Inhibition kinetic analyses demonstrated that MOA competitively inhibited UGT1A1-catalyzed NHPH-O-glucuronidation in both hUGT1A1 and HLM, with Ki values of 0.52 muM and 1.22 muM, respectively.	nhph-o	91-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
34860573-0	2022	All You Need to Know About UGT1A1 Genetic Testing for Patients Treated With Irinotecan: A Practitioner-Friendly Guide.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
34860573-2	2022	Severe neutropenia and diarrhea are common dose-limiting toxicities of irinotecan-based therapy, and UGT1A1 polymorphisms are one of the major risk factors of these toxicities.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
34860573-3	2022	In 2005, the US Food and Drug Administration revised the drug label to indicate that patients with UGT1A1*28 homozygous genotype should receive a decreased dose of irinotecan.	Irinotecan	164-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
34926449-7	2021	In this study, we demonstrate that arbutin has a protective effect on alpha-naphthylisothiocyanate-induced cholestasis via upregulation of the levels of FXR and downstream enzymes associated with bile acid homeostasis such as Bsep, Ntcp, and Sult2a1, as well as Ugt1a1.	Arbutin	35-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	262-268
34320604-3	2021	This case report demonstrates in vivo the finding of previous in-vitro research suggesting that the UGT1A1 7/7 mutation most commonly associated with Gilbert"s syndrome may result in decreased clozapine excretion.	Clozapine	193-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
34847314-4	2021	Additional, well-planned trials of the UGT1A1 genotype-based approach to irinotecan therapy are predicted to reduce adverse drug events in people with the UGT1A1*28/*28 genotypes and improve treatment efficacy in the rest of the patients, which might be cost-effective.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
34536821-0	2021	Upregulation of UGT1A1 expression by ursolic acid and oleanolic acid via the inhibition of the PKC/NF-kappaB signaling pathway.	ursolic acid	37-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
34807779-1	2022	UDP-glucuronyltransferase 1A1 (UGT1A1) is a member of the Phase II metabolic enzyme family and the only enzyme that can metabolize detoxified bilirubin.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-29
34807779-1	2022	UDP-glucuronyltransferase 1A1 (UGT1A1) is a member of the Phase II metabolic enzyme family and the only enzyme that can metabolize detoxified bilirubin.	Bilirubin	142-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
34192355-6	2021	RESULTS: Our data indicated that dabrafenib had a broad inhibitory effect on 4-MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib can increase the area under curve (AUC) of co-administered drug.	dabrafenib	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
34192355-7	2021	CONCLUSIONS: Dabrafenib is a strong inhibitor of several UGTs and the co-administration of dabrafenib with drugs primarily metabolized by UGT1A1, 1A7, 1A8, or 1A9 may induce potential DDIs.	dabrafenib	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
34192355-7	2021	CONCLUSIONS: Dabrafenib is a strong inhibitor of several UGTs and the co-administration of dabrafenib with drugs primarily metabolized by UGT1A1, 1A7, 1A8, or 1A9 may induce potential DDIs.	dabrafenib	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
34278601-16	2021	Most PHSF patients have UGT1A1 deficiency, which may be the target of rifampicin.	Rifampin	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
34794220-1	2021	Objective: To investigate the correlation between UGT1A1 polymorphisms and the irinotecan plus S-1 regimen-induced toxicities in Chinese advanced esophageal squamous cell carcinoma (ESCC) patients.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
34794220-5	2021	Irinotecan plus S-1 regimen-induced toxicities of patients with different UGT1A1 polymorphisms were observed.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
34327766-0	2021	Impact of UGT1A1 Genotype on the Efficacy and Safety of Irinotecan-based Chemotherapy in Metastatic Colorectal Cancer.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
34327766-2	2021	We evaluated the associations between the UGT1A1 genotype linked to adverse events - caused by irinotecan - and the efficacy and safety of mXELIRI and FOLFIRI.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
34327766-2	2021	We evaluated the associations between the UGT1A1 genotype linked to adverse events - caused by irinotecan - and the efficacy and safety of mXELIRI and FOLFIRI.	mxeliri	139-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
34327766-2	2021	We evaluated the associations between the UGT1A1 genotype linked to adverse events - caused by irinotecan - and the efficacy and safety of mXELIRI and FOLFIRI.	FOLFIRI regimen	151-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
34866848-2	2021	In most cases, GS is associated with the UGT1A1*28 polymorphism of UGT1A1 gene coding the enzyme bilirubin uridine diphosphate glucuronosyltransferase (UGT-1A) which plays a key role in the bilirubin metabolism.	Bilirubin	97-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
34866848-2	2021	In most cases, GS is associated with the UGT1A1*28 polymorphism of UGT1A1 gene coding the enzyme bilirubin uridine diphosphate glucuronosyltransferase (UGT-1A) which plays a key role in the bilirubin metabolism.	Bilirubin	97-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
34866848-2	2021	In most cases, GS is associated with the UGT1A1*28 polymorphism of UGT1A1 gene coding the enzyme bilirubin uridine diphosphate glucuronosyltransferase (UGT-1A) which plays a key role in the bilirubin metabolism.	Bilirubin	190-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
34866848-2	2021	In most cases, GS is associated with the UGT1A1*28 polymorphism of UGT1A1 gene coding the enzyme bilirubin uridine diphosphate glucuronosyltransferase (UGT-1A) which plays a key role in the bilirubin metabolism.	Bilirubin	190-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
34866848-7	2021	Conclusions: Despite the fact that the level of serum bilirubin increases with the rise in the number of additional TA dinucleotides in the UGT1A1 gene promoter tests of clinical manifestations only (jaundice, fatigue, sleep disturbances, nausea, belching, and so on) and increased bilirubin levels in patients with normal liver function do not allow unequivocally diagnose GS.	Bilirubin	54-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
34866848-7	2021	Conclusions: Despite the fact that the level of serum bilirubin increases with the rise in the number of additional TA dinucleotides in the UGT1A1 gene promoter tests of clinical manifestations only (jaundice, fatigue, sleep disturbances, nausea, belching, and so on) and increased bilirubin levels in patients with normal liver function do not allow unequivocally diagnose GS.	ta dinucleotides	116-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
34536821-0	2021	Upregulation of UGT1A1 expression by ursolic acid and oleanolic acid via the inhibition of the PKC/NF-kappaB signaling pathway.	Oleanolic Acid	54-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
34536821-8	2021	Phorbol 12-myristate 13-acetate (PMA) and lipopolysaccharide (LPS), the agonists of PKC and NF-kappaB signaling, respectively, significantly inhibit hp65-mediated UGT1A1 luciferase activity.	Tetradecanoylphorbol Acetate	0-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
34536821-8	2021	Phorbol 12-myristate 13-acetate (PMA) and lipopolysaccharide (LPS), the agonists of PKC and NF-kappaB signaling, respectively, significantly inhibit hp65-mediated UGT1A1 luciferase activity.	Tetradecanoylphorbol Acetate	33-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
34536821-10	2021	PMA and LPS do not affect UGT1A1 activity in p65-silenced HepG2 cells; however, UA and OA mildly influence UGT1A1 expression in these cells.	Tetradecanoylphorbol Acetate	0-3	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
34698602-3	2021	UGT1A1 catalyzed beta-estradiol 3-beta-D-glucuronide formation showed allosteric sigmoidal kinetics in all enzyme systems; while UGT1A3 catalyzed CDCA 24-acyl-beta-D-glucuronide formation exhibited Michaelis-Menten kinetics in HLM, substrate inhibition kinetics in HIM and rUGT systems.	Estradiol	17-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34698602-3	2021	UGT1A1 catalyzed beta-estradiol 3-beta-D-glucuronide formation showed allosteric sigmoidal kinetics in all enzyme systems; while UGT1A3 catalyzed CDCA 24-acyl-beta-D-glucuronide formation exhibited Michaelis-Menten kinetics in HLM, substrate inhibition kinetics in HIM and rUGT systems.	3-beta-d-glucuronide	32-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34698602-3	2021	UGT1A1 catalyzed beta-estradiol 3-beta-D-glucuronide formation showed allosteric sigmoidal kinetics in all enzyme systems; while UGT1A3 catalyzed CDCA 24-acyl-beta-D-glucuronide formation exhibited Michaelis-Menten kinetics in HLM, substrate inhibition kinetics in HIM and rUGT systems.	24-acyl-beta-d-glucuronide	151-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34703007-6	2022	SN-38 clearance was influenced by rs887829 in UGT1A1, pre-treatment total bilirubin, and EGFR rare variant burden.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
34703007-7	2022	Within each UGT1A1 genotype group, elevated pre-treatment total bilirubin and/or presence of at least one rare variant in EGFR resulted in significantly lower SN-38 clearance.	Irinotecan	159-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
34814402-1	2021	Gilbert"s syndrome is a kind of benign inherited disease of bilirubin binding disorder, mainly due to the homozygous polymorphism A(TA)7TAA in the promoter of the gene for uridine diphosphate -glucuronosyltransferase 1A1 (UGT1A1), which is a TA insertion into the promoter, designated as UGT1A1*28, with UGT activity reduction to 30% of the normal value.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	172-220
34814402-1	2021	Gilbert"s syndrome is a kind of benign inherited disease of bilirubin binding disorder, mainly due to the homozygous polymorphism A(TA)7TAA in the promoter of the gene for uridine diphosphate -glucuronosyltransferase 1A1 (UGT1A1), which is a TA insertion into the promoter, designated as UGT1A1*28, with UGT activity reduction to 30% of the normal value.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
34814402-1	2021	Gilbert"s syndrome is a kind of benign inherited disease of bilirubin binding disorder, mainly due to the homozygous polymorphism A(TA)7TAA in the promoter of the gene for uridine diphosphate -glucuronosyltransferase 1A1 (UGT1A1), which is a TA insertion into the promoter, designated as UGT1A1*28, with UGT activity reduction to 30% of the normal value.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	288-294
34528449-3	2021	Results: A novel cis-eQTL, rs28967009, was identified for UGT1A1, which is predicted to upregulate UGT1A1 expression thereby potentially affecting the metabolism of dolutegravir and irinotecan, which are extensively prescribed in SA for HIV and colorectal cancer treatment, respectively.	dolutegravir	165-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
34486919-4	2021	Furthermore, prospective trials have shown that patients harboring the UGT1A1 *1/*1 and *1/*28 genotypes can tolerate higher doses of irinotecan, which may in turn impact on a better outcome.	Irinotecan	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
34486919-5	2021	Upfront UGT1A1 genotyping could therefore be a usefulness strategy in order to individualize irinotecan dosing, but consensus on the recommended dose based on the UGT1A1 genotype is still lacking.	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
34486919-8	2021	EXPERT OPINION: Implementation of UGT1A1*28 and UGT1A1*6 genotyping in clinical practice is a first step toward personalizing irinotecan therapy.	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
34486919-8	2021	EXPERT OPINION: Implementation of UGT1A1*28 and UGT1A1*6 genotyping in clinical practice is a first step toward personalizing irinotecan therapy.	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	ticagrelor-o-glucuronide	187-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
34528449-3	2021	Results: A novel cis-eQTL, rs28967009, was identified for UGT1A1, which is predicted to upregulate UGT1A1 expression thereby potentially affecting the metabolism of dolutegravir and irinotecan, which are extensively prescribed in SA for HIV and colorectal cancer treatment, respectively.	dolutegravir	165-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
34528449-3	2021	Results: A novel cis-eQTL, rs28967009, was identified for UGT1A1, which is predicted to upregulate UGT1A1 expression thereby potentially affecting the metabolism of dolutegravir and irinotecan, which are extensively prescribed in SA for HIV and colorectal cancer treatment, respectively.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
34528449-3	2021	Results: A novel cis-eQTL, rs28967009, was identified for UGT1A1, which is predicted to upregulate UGT1A1 expression thereby potentially affecting the metabolism of dolutegravir and irinotecan, which are extensively prescribed in SA for HIV and colorectal cancer treatment, respectively.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
34528449-4	2021	Conclusion: As increased UGT1A1 expression could affect the clinical outcome of dolutegravir and irinotecan treatment by increasing drug clearance, patients with the rs28967009A variant may require increased drug doses to reach therapeutic levels or should be prescribed alternative drugs.	dolutegravir	80-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
34528449-4	2021	Conclusion: As increased UGT1A1 expression could affect the clinical outcome of dolutegravir and irinotecan treatment by increasing drug clearance, patients with the rs28967009A variant may require increased drug doses to reach therapeutic levels or should be prescribed alternative drugs.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
34573035-0	2021	Bilirubin Links HO-1 and UGT1A1*28 Gene Polymorphisms to Predict Cardiovascular Outcome in Patients Receiving Maintenance Hemodialysis.	Bilirubin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
34575495-2	2021	Resveratrol enantiomers showed stereoselective inhibition of CYP2C9, CYP3A, and UGT1A1.	Resveratrol	0-11	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
34575495-5	2021	Trans-resveratrol noncompetitively inhibited CYP3A and UGT1A1 activities with Ki values of 23.8 and 27.4 muM, respectively.	Resveratrol	0-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
34575495-8	2021	This information helped the prediction of food drug interaction potentials between resveratrol and co-administered drugs which are mainly metabolized by UGT1A1, CYP1A2, CYP2C19, CYP2E1, and CYP3A.	Resveratrol	83-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
34572750-9	2021	Nine patients with toxicity-associated pharmacogenomic variants were treated with a relevant medication: seven UGT1A1 intermediate metabolizers were treated with irinotecan, one intermediate DPYD metabolizer was treated with 5-fluorouracil, and one TPMT poor metabolizer was treated with mercaptopurine.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
34572750-11	2021	One UGT1A1 heterozygote died after a single dose of irinotecan due to irinotecan-related adverse effects.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
34572750-11	2021	One UGT1A1 heterozygote died after a single dose of irinotecan due to irinotecan-related adverse effects.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
34573035-1	2021	Serum bilirubin levels, which are determined by a complex interplay of various enzymes, including heme oxygenase-1 (HO-1) and uridine diphosphate-glucuronosyl transferase (UGT1A1), may be protective against progression of cardiovascular disease (CVD) in hemodialysis patients.	Bilirubin	6-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	172-178
34573035-3	2021	This retrospective study enrolled 1080 prevalent hemodialysis patients and the combined genetic polymorphisms of HO-1 and UGT1A1 on serum bilirubin were analyzed.	Bilirubin	138-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
34909672-4	2021	The metabolism pathways of dolutegravir and bictegravir are similar, both including CYP3A and UGT1A1, and both agents are substrates to different drug transporters.	dolutegravir	27-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
34575401-5	2021	Drug-drug interactions (DDIs) of UGT1A1 substrates dolutegravir and raltegravir with UGT1A1 inhibitor atazanavir have been simulated, and the role of intestinal metabolism in these clinical DDIs examined.	dolutegravir	51-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
34575401-5	2021	Drug-drug interactions (DDIs) of UGT1A1 substrates dolutegravir and raltegravir with UGT1A1 inhibitor atazanavir have been simulated, and the role of intestinal metabolism in these clinical DDIs examined.	Raltegravir Potassium	68-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
34575401-5	2021	Drug-drug interactions (DDIs) of UGT1A1 substrates dolutegravir and raltegravir with UGT1A1 inhibitor atazanavir have been simulated, and the role of intestinal metabolism in these clinical DDIs examined.	Raltegravir Potassium	68-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
34575401-5	2021	Drug-drug interactions (DDIs) of UGT1A1 substrates dolutegravir and raltegravir with UGT1A1 inhibitor atazanavir have been simulated, and the role of intestinal metabolism in these clinical DDIs examined.	Atazanavir Sulfate	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
34575401-5	2021	Drug-drug interactions (DDIs) of UGT1A1 substrates dolutegravir and raltegravir with UGT1A1 inhibitor atazanavir have been simulated, and the role of intestinal metabolism in these clinical DDIs examined.	Atazanavir Sulfate	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
34909672-4	2021	The metabolism pathways of dolutegravir and bictegravir are similar, both including CYP3A and UGT1A1, and both agents are substrates to different drug transporters.	bictegravir	44-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
34117260-0	2021	A UGT1A1 variant is associated with serum total bilirubin levels, which are causal for hypertension in African-ancestry individuals.	Bilirubin	48-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	2-8
34149888-0	2021	Inhibitory effects of quercetin and its major metabolite quercetin-3-O-beta-D-glucoside on human UDP-glucuronosyltransferase 1A isoforms by liquid chromatography-tandem mass spectrometry.	Quercetin	22-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-127
34149888-0	2021	Inhibitory effects of quercetin and its major metabolite quercetin-3-O-beta-D-glucoside on human UDP-glucuronosyltransferase 1A isoforms by liquid chromatography-tandem mass spectrometry.	isoquercitrin	57-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-127
34149888-6	2021	Preliminary screening experiments indicated that quercetin exhibited stronger inhibitory effects on UGT1A1, UGT1A3, UGT1A6 and UGT1A9 enzymes than Q3GA.	Quercetin	49-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
34149888-8	2021	Quercetin exerted non-competitive inhibition on UGT1A1 and UGT1A6, with half maximal inhibitory concentration (IC50) values of 7.47 and 7.07 microM and inhibition kinetic parameter (Ki) values of 2.18 and 28.87 microM, respectively.	Quercetin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
34149888-11	2021	In the present study, quercetin was a moderate inhibitor of UGT1A1 and UGT1A3, a weak inhibitor of UGT1A6, and a strong inhibitor on UGT1A9.	Quercetin	22-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
34149888-12	2021	The results of the present study suggested potential HDIs that may occur following quercetin co-administration with drugs that are mainly metabolized by UGT1A1, UGT1A3 and UGT1A9 enzymes.	Quercetin	83-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-159
34085382-7	2021	YZH and its two active ingredients, namely baicalin (BCL) and 4"-hydroxyacetophenone (4-HT), up-regulated the mRNA expression of AhR target genes ( CYP1A1 and UGT1A1)  and increased nuclear protein levels of AhR in HepG2 cells.	baicalin	43-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
34085382-7	2021	YZH and its two active ingredients, namely baicalin (BCL) and 4"-hydroxyacetophenone (4-HT), up-regulated the mRNA expression of AhR target genes ( CYP1A1 and UGT1A1)  and increased nuclear protein levels of AhR in HepG2 cells.	baicalin	53-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
34085382-7	2021	YZH and its two active ingredients, namely baicalin (BCL) and 4"-hydroxyacetophenone (4-HT), up-regulated the mRNA expression of AhR target genes ( CYP1A1 and UGT1A1)  and increased nuclear protein levels of AhR in HepG2 cells.	4-hydroxyacetophenone	62-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
34085382-7	2021	YZH and its two active ingredients, namely baicalin (BCL) and 4"-hydroxyacetophenone (4-HT), up-regulated the mRNA expression of AhR target genes ( CYP1A1 and UGT1A1)  and increased nuclear protein levels of AhR in HepG2 cells.	4-hydroxyacetophenone	86-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
34117260-5	2021	The SNP rs887829 (UGT1A1) was significantly associated with TBIL levels (effect allele (T) frequency = 0.49, beta (SE) = 0.59 (0.04), p = 9.13 x 10-54).	tbil	60-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
34117260-9	2021	Our finding confirms that UGT1A1 influences bilirubin levels.	Bilirubin	44-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
34093191-9	2021	Results: In ATV-treated patients, hyperbilirubinemia (total bilirubin >1.2 mg/dl) had the main incidence (61.11%), and moderate and severe hyperbilirubinemia (total bilirubin >1.9 mg/dl) were statistically associated with UGT1A1*28 in recessive and codominant inheritance models (OR = 16.33, p = 0.028 and OR = 10.82, p = 0.036, respectively).	Atazanavir Sulfate	12-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
34074250-0	2021	UGT1A1 mutation association with increased bilirubin levels and severity of unconjugated hyperbilirubinemia in ABO incompatible newborns of China.	Bilirubin	43-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34074250-2	2021	Uridine diphosphate glucuronosyltransferase isoenzyme (UGT1A1) glucuronidates bilirubin and converts the toxic form of bilirubin to its nontoxic form.	Uridine Diphosphate	0-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
34074250-2	2021	Uridine diphosphate glucuronosyltransferase isoenzyme (UGT1A1) glucuronidates bilirubin and converts the toxic form of bilirubin to its nontoxic form.	Bilirubin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
34074250-2	2021	Uridine diphosphate glucuronosyltransferase isoenzyme (UGT1A1) glucuronidates bilirubin and converts the toxic form of bilirubin to its nontoxic form.	Bilirubin	119-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
34074250-6	2021	UGT1A1 c.211 G > A mutation (UGT1A1*6, p.Arg71Gly, rs4148323) was significantly associated with the increased bilirubin level in ABO HDNs, after adjusted by age, sex and feeding method (P = 0.019 for TBIL, P = 0.02 for IBIL).	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34074250-6	2021	UGT1A1 c.211 G > A mutation (UGT1A1*6, p.Arg71Gly, rs4148323) was significantly associated with the increased bilirubin level in ABO HDNs, after adjusted by age, sex and feeding method (P = 0.019 for TBIL, P = 0.02 for IBIL).	Bilirubin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
34074250-6	2021	UGT1A1 c.211 G > A mutation (UGT1A1*6, p.Arg71Gly, rs4148323) was significantly associated with the increased bilirubin level in ABO HDNs, after adjusted by age, sex and feeding method (P = 0.019 for TBIL, P = 0.02 for IBIL).	tbil	200-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34074250-6	2021	UGT1A1 c.211 G > A mutation (UGT1A1*6, p.Arg71Gly, rs4148323) was significantly associated with the increased bilirubin level in ABO HDNs, after adjusted by age, sex and feeding method (P = 0.019 for TBIL, P = 0.02 for IBIL).	ibil	219-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34093191-3	2021	UGT1A1*28 and CYP2B6 c.516G>T have been proposed to be related with higher toxicity by ATV and EFV, respectively.	Atazanavir Sulfate	87-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34093191-3	2021	UGT1A1*28 and CYP2B6 c.516G>T have been proposed to be related with higher toxicity by ATV and EFV, respectively.	efavirenz	95-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34093191-9	2021	Results: In ATV-treated patients, hyperbilirubinemia (total bilirubin >1.2 mg/dl) had the main incidence (61.11%), and moderate and severe hyperbilirubinemia (total bilirubin >1.9 mg/dl) were statistically associated with UGT1A1*28 in recessive and codominant inheritance models (OR = 16.33, p = 0.028 and OR = 10.82, p = 0.036, respectively).	Bilirubin	165-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
34093191-13	2021	Conclusion: Our findings suggest that after treatment with ATV or EFV, UGT1A1*28 and CYP2B6 c.516G>T influence the appearance of moderate-to-severe hyperbilirubinemia and CNS toxicity, respectively.	Atazanavir Sulfate	59-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
35512135-7	2022	Of nine polymorphisms previously associated with dolutegravir pharmacokinetics, the lowest P-value with AUCVAR was UGT1A1 rs887829 (P = 1.8 x 10-4), which was also associated with log10 bilirubin (P = 8.6 x 10-13).	dolutegravir	49-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
34272713-9	2021	Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport.	Bilirubin	126-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
34272713-9	2021	Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport.	Bilirubin	208-217	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	192-198
35415893-2	2022	The aim of this clinical study was to evaluate the safety, efficacy and pharmacokinetics of a novel regimen comprised of metronomic oxaliplatin (O), chronomodulated capecitabine (X) and UGT1A1 genotype-guided dosing of irinotecan (IRI) (OXIRI) as well as its immunomodulatory effects.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-192
35415893-7	2022	UGT1A1-genotype directed dosing resulted in similar exposure levels of irinotecan, SN-38 and SN-38G in all patients.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35415893-7	2022	UGT1A1-genotype directed dosing resulted in similar exposure levels of irinotecan, SN-38 and SN-38G in all patients.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35415893-7	2022	UGT1A1-genotype directed dosing resulted in similar exposure levels of irinotecan, SN-38 and SN-38G in all patients.	7-ethyl-10-hydroxycamptothecin beta-glucuronide	93-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35633386-7	2022	RESULTS: The multivariate regression model revealed that patients who carried one or more detrimental allelic variant (CYP2D6, CYP3A5, and UGT1A1) showed a tendency toward a higher galantamine adjusted Cpss (B = 34.559, 95% CI = 0.741-68.377, p value = 0.045).	Galantamine	181-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	139-145
35633386-9	2022	UGT1A1 mutant alleles and non-genetic factors including concomitant use of statin drugs and higher education level can attenuate therapeutic outcomes of galantamine.	Galantamine	153-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35633386-10	2022	CONCLUSION: Pharmacokinetic-related genes including CYP2D6*10 and UGT1A1 mutant alleles were significantly associated with galantamine adjusted Cpss and cognitive function.	Galantamine	123-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
34609801-3	2021	It happens as a result of an error in UGT1A1 enzyme which can cause high unconjugated bilirubin levels.	Bilirubin	86-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
35527687-2	2022	The expression of UGT1A1 is relatively managed by a polymorphic dinucleotide repeat inside the promoter TATA box consisting of 5-8 copies of a TA repeat.	Dinucleoside Phosphates	64-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
35637361-1	2022	BACKGROUND: UGT1A1 polymorphisms should be considered when using irinotecan-containing regimens, especially in patients with a double-variant-type (DV), including homozygous for UGT1A1*28 and UGT1A1*6 and heterozygous for both UGT1A1*28 and UGT1A1*6.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
35177165-1	2022	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility and toxicity of patients to irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-47
35512135-7	2022	Of nine polymorphisms previously associated with dolutegravir pharmacokinetics, the lowest P-value with AUCVAR was UGT1A1 rs887829 (P = 1.8 x 10-4), which was also associated with log10 bilirubin (P = 8.6 x 10-13).	Bilirubin	186-195	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
35177165-1	2022	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility and toxicity of patients to irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
35506159-0	2022	Association of UGT1A1*6,*28 or ABCC2 c.3972C>T genetic polymorphisms with irinotecan induced toxicity in Asian cancer patients: Meta-analysis.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
35177165-2	2022	This retrospective, observational study compared the clinical outcomes and adverse events (AEs) in RAS wild-type metastatic colorectal cancer (mCRC) patients treated with cetuximab or bevacizumab plus FOLFIRI with UGT1A1 genotyping and irinotecan dose escalation as the first-line therapy.	Irinotecan	236-246	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	214-220
35177165-5	2022	All patients received irinotecan dose escalation based on UGT1A1 genotyping.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
35177165-10	2022	Our results revealed that patients with wild-type RAS mCRC, regardless of biologics, with UGT1A1 genotyping can tolerate escalated doses of irinotecan and potentially achieve a more favorable clinical outcome without significantly increased toxicity.	Irinotecan	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
35506159-3	2022	It was aimed to assess the aggregated risk of neutropenia or diarrhea in Asian cancer patients taking irinotecan and inherited UGT1A1*6, UGT1A1*28 or ABCC2 c.3972C>T genetic variants.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
35506159-9	2022	Both UGT1A1*6 and UGT1A1*28 genetic variants should be screened in Asian cancer patients to reduce substantially irinotecan induced severe toxicities.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
35506159-9	2022	Both UGT1A1*6 and UGT1A1*28 genetic variants should be screened in Asian cancer patients to reduce substantially irinotecan induced severe toxicities.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
35241486-10	2022	As a commonly used herbal products rich in flavonoids, Shuang-huang-lian injections (SHL), easily lead to symptoms of liver injury (e.g., jaundice) owing to significant inhibition of hUGT1A1-mediated bilirubin glucuronidation by its flavonoid components (i.e., baicalein, baicalin, hyperoside).	Bilirubin	200-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-190
35501760-6	2022	To the combined of UGT1A1, total bilirubin levels in homozygous variant were higher significantly than heterozygous variant and wild type (P = 0.002, P = 0.003, respectively).	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
35233973-5	2022	We also assessed the impact of UGT1A1 gene polymorphisms, which are involved in irinotecan metabolism, on outcomes and toxicity.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
35233973-7	2022	Six (15%) patients (UGT1A1 wild-type (n = 2) and heterozygous (n = 4)) showed objective responses, including partial response (n = 1), tumor shrinkage (n = 4), and improved findings on their MIBG scan (n = 1).	3-Iodobenzylguanidine	191-195	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35241486-0	2022	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by the Popular Flavonoids Baicalein, Baicalin and Hyperoside is responsible for Herbs (Shuang-huang-lian) -Induced Jaundice.	Bilirubin	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35241486-0	2022	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by the Popular Flavonoids Baicalein, Baicalin and Hyperoside is responsible for Herbs (Shuang-huang-lian) -Induced Jaundice.	Flavonoids	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35241486-10	2022	As a commonly used herbal products rich in flavonoids, Shuang-huang-lian injections (SHL), easily lead to symptoms of liver injury (e.g., jaundice) owing to significant inhibition of hUGT1A1-mediated bilirubin glucuronidation by its flavonoid components (i.e., baicalein, baicalin, hyperoside).	Flavonoids	233-242	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-190
35241486-0	2022	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by the Popular Flavonoids Baicalein, Baicalin and Hyperoside is responsible for Herbs (Shuang-huang-lian) -Induced Jaundice.	baicalein	88-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35241486-10	2022	As a commonly used herbal products rich in flavonoids, Shuang-huang-lian injections (SHL), easily lead to symptoms of liver injury (e.g., jaundice) owing to significant inhibition of hUGT1A1-mediated bilirubin glucuronidation by its flavonoid components (i.e., baicalein, baicalin, hyperoside).	baicalein	261-270	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-190
35241486-0	2022	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by the Popular Flavonoids Baicalein, Baicalin and Hyperoside is responsible for Herbs (Shuang-huang-lian) -Induced Jaundice.	baicalin	99-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35241486-10	2022	As a commonly used herbal products rich in flavonoids, Shuang-huang-lian injections (SHL), easily lead to symptoms of liver injury (e.g., jaundice) owing to significant inhibition of hUGT1A1-mediated bilirubin glucuronidation by its flavonoid components (i.e., baicalein, baicalin, hyperoside).	baicalin	272-280	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-190
35241486-0	2022	Inhibition of Human UGT1A1-Mediated Bilirubin Glucuronidation by the Popular Flavonoids Baicalein, Baicalin and Hyperoside is responsible for Herbs (Shuang-huang-lian) -Induced Jaundice.	hyperoside	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35241486-3	2022	The aim of this paper was to explore the mechanism of Shuang-huang-lian injections (SHL) and its major constituents-induced jaundice via inhibiting human UDP-glucuronosyltransferases1A1 (hUGT1A1)-mediated bilirubin glucuronidation.	Bilirubin	205-214	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-194
35241486-10	2022	As a commonly used herbal products rich in flavonoids, Shuang-huang-lian injections (SHL), easily lead to symptoms of liver injury (e.g., jaundice) owing to significant inhibition of hUGT1A1-mediated bilirubin glucuronidation by its flavonoid components (i.e., baicalein, baicalin, hyperoside).	hyperoside	282-292	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-190
35241486-7	2022	Both inhibition kinetics assays and molecular docking simulations suggested that SHL, BAI, BA, and HYP significantly inhibited hUGT1A1-mediated bilirubin glucuronidation via a mixed-type inhibition.	Bilirubin	144-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-134
35445479-6	2022	SN-38 is inactivated by UGT1A1 enzymes.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
35241486-8	2022	Collectively, some naturally occurring flavonoids (BAI, BA and HYP) in SHL have been identified as the inhibitors against hUGT1A1-mediated bilirubin glucuronidation, which well-explains the bilirubin-related ADRs or malady triggered by SHL in clinical settings.	Flavonoids	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
35241486-8	2022	Collectively, some naturally occurring flavonoids (BAI, BA and HYP) in SHL have been identified as the inhibitors against hUGT1A1-mediated bilirubin glucuronidation, which well-explains the bilirubin-related ADRs or malady triggered by SHL in clinical settings.	Bilirubin	139-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
35241486-8	2022	Collectively, some naturally occurring flavonoids (BAI, BA and HYP) in SHL have been identified as the inhibitors against hUGT1A1-mediated bilirubin glucuronidation, which well-explains the bilirubin-related ADRs or malady triggered by SHL in clinical settings.	Bilirubin	190-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
35241486-10	2022	As a commonly used herbal products rich in flavonoids, Shuang-huang-lian injections (SHL), easily lead to symptoms of liver injury (e.g., jaundice) owing to significant inhibition of hUGT1A1-mediated bilirubin glucuronidation by its flavonoid components (i.e., baicalein, baicalin, hyperoside).	Flavonoids	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-190
35147853-0	2022	Prediction of Drug-Drug Interaction Between Dabrafenib and Irinotecan via UGT1A1-Mediated Glucuronidation.	dabrafenib	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
35147853-0	2022	Prediction of Drug-Drug Interaction Between Dabrafenib and Irinotecan via UGT1A1-Mediated Glucuronidation.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
35147853-4	2022	METHODS: Recombinant human uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and human liver microsomes (HLMs) were employed to catalyze the glucuronidation of SN-38 in vitro.	Irinotecan	167-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-74
35147853-4	2022	METHODS: Recombinant human uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and human liver microsomes (HLMs) were employed to catalyze the glucuronidation of SN-38 in vitro.	Irinotecan	167-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
35147853-6	2022	RESULTS: Dabrafenib noncompetitively inhibited SN-38 glucuronidation in pooled HLMs and recombinant UGT1A1 with unbound inhibitor constant (Ki,u) values of 12.43 +- 0.28 and 3.89 +- 0.40 muM, respectively.	dabrafenib	9-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
35147853-6	2022	RESULTS: Dabrafenib noncompetitively inhibited SN-38 glucuronidation in pooled HLMs and recombinant UGT1A1 with unbound inhibitor constant (Ki,u) values of 12.43 +- 0.28 and 3.89 +- 0.40 muM, respectively.	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
35147853-8	2022	However, the ratios of intra-enterocyte concentration of dabrafenib to Ki,u ((I)gut/Ki,u) are 2.73 and 8.72 in HLMs and recombinant UGT1A1, respectively, indicating a high risk of intestinal DDI when dabrafenib was used in combination with irinotecan.	dabrafenib	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
35147853-9	2022	CONCLUSION: Dabrafenib is a potent noncompetitive inhibitor of UGT1A1 and may bring potential risk of DDI when combined with irinotecan.	dabrafenib	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
35147853-9	2022	CONCLUSION: Dabrafenib is a potent noncompetitive inhibitor of UGT1A1 and may bring potential risk of DDI when combined with irinotecan.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
35149777-0	2022	UGT1A1 genetic variants are associated with increases in bilirubin levels in rheumatoid arthritis patients treated with sarilumab.	Bilirubin	57-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35149777-5	2022	Variants in the UGT1A1 gene were strongly associated with maximum bilirubin elevations in sarilumab-treated patients (rs4148325; p = 2.88 x 10-41) but were not associated with aminotransferase elevations.	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
35149777-7	2022	These findings suggest that most bilirubin increases during sarilumab treatment are related to genetic variation in UGT1A1 rather than underlying liver injury.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
35498511-0	2022	Clinical Outcomes of Patients with Peritoneal Metastasis-Only Colorectal Cancer Treated with First-Line Bevacizumab and FOLFIRI Through Irinotecan Dose Escalation According to UGT1A1 Polymorphism: Compared to Liver Metastasis-Only, and Lung Metastasis-Only.	FOLFIRI regimen	120-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
35498511-8	2022	All patients with PC-only CRC were treated with first-line bevacizumab and FOLFIRI, and the irinotecan dose escalation depended on UGT1A1 polymorphism.	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
35498511-13	2022	Conclusion: Our study revealed that in patients with PC-only mCRC treatment of first-line bevacizumab and FOLFIRI through irinotecan dose escalation according to UGT1A1 polymorphism could confer such patients with comparable outcomes to that of patients with LiM-only and LuM-only mCRC.	FOLFIRI regimen	106-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
35498511-13	2022	Conclusion: Our study revealed that in patients with PC-only mCRC treatment of first-line bevacizumab and FOLFIRI through irinotecan dose escalation according to UGT1A1 polymorphism could confer such patients with comparable outcomes to that of patients with LiM-only and LuM-only mCRC.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
35436954-2	2022	BACKGROUND: Several mutations of bilirubin uridine diphosphate-glucuronosyltransferase gene (UGT1A1) have been reported in patients with unconjugated hyperbilirubinemia.	Bilirubin	33-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
35061524-0	2022	Precision Medicine: UGT1A1 Genotyping to Better Manage Irinotecan-Induced Toxicity.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35226656-2	2022	Mutations in the UGT1A1 gene can be associated with increased toxicity from irinotecan-based chemotherapy.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
35063619-4	2022	Myricetin exhibited strong inhibitory effects against UGT1A1, 1A3, 1A6, 1A7, 1A10 (IC50 < 10 muM) with non-competitive inhibition type, while serving as a moderate inhibitor against UGT1A9 and 2B7 (IC50 range from 25 to 29 muM) with competitive and mixed inhibition type, respectively.	myricetin	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
35063619-7	2022	The quantitative prediction in vivo of inhibition on gastrointestinal UGTs by myricetin showed that the inhibition against UGT1A1, 1A3, 1A6, 1A7, 1A9, 1A10 and 2B7 would likely occur with high risk.	myricetin	78-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
35226656-5	2022	Genetic testing identified a mutation in the UGT1A1 gene associated with increased toxicity to irinotecan, and the EIA tests performed for evaluation of C. difficile toxins A and B showed repeatedly negative results.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
34996412-1	2022	BACKGROUND: Pharmacogenetic (PGx) testing for germline variants in the DPYD and UGT1A1 genes can be used to guide fluoropyrimidine and irinotecan dosing, respectively.	2-fluoropyrimidine	114-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
34654938-3	2022	Patients with genotype UGT1A1*6 (exon 1, 211G > A) treated with the antineoplastic drug SN-38 have been reported to exhibit decreased glucuronide conjugation and increased incidence of intestinal toxicity and its severe side effects, including severe diarrhea.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
34654938-3	2022	Patients with genotype UGT1A1*6 (exon 1, 211G > A) treated with the antineoplastic drug SN-38 have been reported to exhibit decreased glucuronide conjugation and increased incidence of intestinal toxicity and its severe side effects, including severe diarrhea.	Glucuronides	134-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
34654938-7	2022	The CYP3A4 POR UGT1A1*6 KI-Caco-2 cells were sensitive to SN-38-induced intestinal toxicity.	Irinotecan	58-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
35192750-12	2022	There was no significant difference in the concentration of ALT, AST, cholesterol or LDL between different genotypes.The number of TA-repeats of the UGT1A1 gene affects the increase of total bilirubin and its indirect fraction, including the cases of rare allelic variants (TA<=5, TA>=8), but not the activity of ALT and AST and the lipid profile.	Cholesterol	70-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
35192750-12	2022	There was no significant difference in the concentration of ALT, AST, cholesterol or LDL between different genotypes.The number of TA-repeats of the UGT1A1 gene affects the increase of total bilirubin and its indirect fraction, including the cases of rare allelic variants (TA<=5, TA>=8), but not the activity of ALT and AST and the lipid profile.	Bilirubin	191-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
35264954-5	2022	Further investigations demonstrated that four biflavones including bilobetin, isoginkgetin, sciadopitysin and ginkgetin, are key constituents responsible for hUGT1A1 inhibition in living cells.	biflavones	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-165
35264954-5	2022	Further investigations demonstrated that four biflavones including bilobetin, isoginkgetin, sciadopitysin and ginkgetin, are key constituents responsible for hUGT1A1 inhibition in living cells.	bilobetin	67-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-165
35264954-5	2022	Further investigations demonstrated that four biflavones including bilobetin, isoginkgetin, sciadopitysin and ginkgetin, are key constituents responsible for hUGT1A1 inhibition in living cells.	isoginkgetin	78-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-165
35264954-5	2022	Further investigations demonstrated that four biflavones including bilobetin, isoginkgetin, sciadopitysin and ginkgetin, are key constituents responsible for hUGT1A1 inhibition in living cells.	sciadopitysin	92-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-165
35264954-5	2022	Further investigations demonstrated that four biflavones including bilobetin, isoginkgetin, sciadopitysin and ginkgetin, are key constituents responsible for hUGT1A1 inhibition in living cells.	ginkgetin	110-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-165
35264954-6	2022	These biflavones potently inhibit hUGT1A1 in both human liver microsomes (HLM) and living cells, with the IC50 values ranging from 0.075 to 0.41 muM in living cells.	biflavones	6-16	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
35264954-7	2022	Inhibition kinetic analyses and docking simulations suggested that four tested biflavones potently inhibit hUGT1A1-catalyzed NHPN-O-glucuronidation in HLM via a mixed inhibition manner, showing the K i values ranging from 0.07 to 0.74 muM.	biflavones	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-114
35264954-7	2022	Inhibition kinetic analyses and docking simulations suggested that four tested biflavones potently inhibit hUGT1A1-catalyzed NHPN-O-glucuronidation in HLM via a mixed inhibition manner, showing the K i values ranging from 0.07 to 0.74 muM.	nhpn	125-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-114
35207692-1	2022	Current guidelines recommend pre-therapeutic UGT1A1 genotyping to guide irinotecan dosing, but the usefulness of this approach remains to be clarified.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
34998046-0	2022	UGT1A1 genotype-guided dosing of irinotecan: A prospective safety and cost analysis in poor metaboliser patients.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34998046-1	2022	AIM: To determine the safety, feasibility, pharmacokinetics, and cost of UGT1A1 genotype-guided dosing of irinotecan.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
34998046-2	2022	PATIENTS AND METHODS: In this prospective, multicentre, non-randomised study, patients intended for treatment with irinotecan were pre-therapeutically genotyped for UGT1A1*28 and UGT1A1*93.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
34998046-2	2022	PATIENTS AND METHODS: In this prospective, multicentre, non-randomised study, patients intended for treatment with irinotecan were pre-therapeutically genotyped for UGT1A1*28 and UGT1A1*93.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
34998046-9	2022	Systemic exposure of SN-38 of reduced dosing in UGT1A1 PMs was still slightly higher compared to a standard-dosed irinotecan patient cohort (difference: +32%).	Irinotecan	21-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
34998046-11	2022	CONCLUSION: UGT1A1 genotype-guided dosing significantly reduces the incidence of febrile neutropenia in UGT1A1 PM patients treated with irinotecan, results in a therapeutically effective systemic drug exposure, and is cost-saving.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
34998046-11	2022	CONCLUSION: UGT1A1 genotype-guided dosing significantly reduces the incidence of febrile neutropenia in UGT1A1 PM patients treated with irinotecan, results in a therapeutically effective systemic drug exposure, and is cost-saving.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
34998046-12	2022	Therefore, UGT1A1 genotype-guided dosing of irinotecan should be considered standard of care in order to improve individual patient safety.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
35017453-2	2022	High levels of raltegravir and dolutegravir can potentially cause bilirubin toxicity as they compete for albumin binding and follow the same metabolic pathway through UGT1A1.	Raltegravir Potassium	15-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
35017453-2	2022	High levels of raltegravir and dolutegravir can potentially cause bilirubin toxicity as they compete for albumin binding and follow the same metabolic pathway through UGT1A1.	dolutegravir	31-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
35017453-2	2022	High levels of raltegravir and dolutegravir can potentially cause bilirubin toxicity as they compete for albumin binding and follow the same metabolic pathway through UGT1A1.	Bilirubin	66-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
35281975-6	2022	Results: Results showed that the processes of albumin-bound bilirubin transfer to the hepatocytes, hepatic uptake, and storage via ligandin, hepatic conjugation via uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1), conjugation into the bile via MRP2 represent the main action mechanism of clofibrate that turns it into the bilirubin conjugates and expels it from the bile.	Bilirubin	60-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	214-220
34996412-1	2022	BACKGROUND: Pharmacogenetic (PGx) testing for germline variants in the DPYD and UGT1A1 genes can be used to guide fluoropyrimidine and irinotecan dosing, respectively.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
35000550-3	2021	In vitro, CC-90001 glucuronidation was catalyzed by UGT1A9, UGT1A4, and UGT1A1, while oxidative metabolism was primarily mediated by CYP3A4/5 with minor contributions from CYP1A2, CYP2C9, CYP2B6, and CYP2D6.2.	CC-90001	10-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
34718654-9	2022	Dasabuvir produced strong partial inhibition effect of UGT1A1 and UGT1A9 and relatively complete inhibition of UGT1A6.	dasabuvir	0-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
35370268-0	2022	The Effect of Single-Walled Carbon Nanotubes on UDP-Glucuronosyltransferase 1A Activity in Human Liver.	Carbon	28-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-78
35370268-4	2022	beta-Estradiol 3-glucuronidation, which is catalyzed mainly by UGT1A1, was inhibited by 99 and 76% in the presence of 0.1 mg/mL EC1.5-P- and FH-P-SWCNTs in human liver microsomes, respectively.	Estradiol	0-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
35370268-4	2022	beta-Estradiol 3-glucuronidation, which is catalyzed mainly by UGT1A1, was inhibited by 99 and 76% in the presence of 0.1 mg/mL EC1.5-P- and FH-P-SWCNTs in human liver microsomes, respectively.	5-p	132-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
35370268-5	2022	The observed decrease of free UGT1A1 protein in the enzyme reaction mixture suggests a higher interaction with SWCNTs, and indicates the inhibition of beta-estradiol 3-glucuronidation.	Estradiol	151-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
35356222-0	2022	UGT1A1 Allele Test Not Only Minimizes the Toxicity But Also Maximizes the Therapeutic Effect of Irinotecan in the Treatment of Colorectal Cancer: A Narrative Review.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35356222-2	2022	Adjusting the dose of irinotecan according to the uridine diphosphate glucuronosyltransferase (UGT) 1A1 genotype reflects the principle of individualized and precision medicine, and may improve the chemotherapy response and survival of CRC.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-103
35356222-3	2022	Methods: To summarize the feasibility, efficacy and safety of high dose irinotecan in CRC patients with UGT1A1 wild-type or heterozygous alleles, PubMed, EMBASE, MEDLINE and the Cochrane Central Register of Controlled Trials online databases were searched from the date of creation to October 22, 2021.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
35356222-5	2022	The results indicated that the maximum tolerated dose of irinotecan in CRC patients with UGT1A1 wild-type or heterozygous variant was significantly higher than the conventional recommended dose.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
35356222-6	2022	Chemotherapy based on high dose irinotecan improved the clinical efficacy in mCRC patients with UGT1A1*28 wild-type and heterozygous variant, and the toxicity was tolerated, as reflected in most studies.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
35356222-7	2022	Conclusions: We are optimistic about the application of high dose irinotecan for mCRC patients with UGT1A1*28 wild-type or heterozygous variant, which will provide a relatively clear direction for future research and certain norms for clinical practice.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106